Operator: Welcome to the Taysha Gene Therapies First Quarter 2021 Financial Results and Corporate Update Conference Call. At this time, all participants are in a listen-only mode. Following management’s prepared remarks, we will hold a brief question-and-answer session. As a reminder, this call is being recorded today, May 11, 2021. I will now turn the call over to Dr. Kimberly Lee, Senior Vice President of Corporate Communications and Investor Relations. Please go ahead.

Kimberly Lee: Good morning, and welcome to Taysha’s first quarter 2021 financial results and corporate update conference call. Joining me on today’s call are RA Session II, Taysha’s President, CEO and Founder; Dr. Suyash Prasad, Chief Medical Officer and Head of R&D; and Kamran Alam, Chief Financial Officer. After our formal remarks, we will conduct the question-and-answer session and instructions will follow at that time. Earlier today, Taysha issued a press release announcing financial results for the first quarter ended March 31, 2021. A copy of this press release is available on the company’s website and through our SEC filings. Please note that on today’s call, we will be making forward-looking statements, including statements relating to the safety and efficacy and the therapeutic and commercial potential of our investigational drug candidates. These statements may include the expected timing and results of clinical trials for our drug candidates and the regulatory status and market opportunities for those programs as well as Taysha’s manufacturing plans. This call may also contain forward-looking statements relating to Taysha’s growth and future operating results, discovery and development of drug candidates, strategic alliances and intellectual property as well as matters that are not historical fact or information. Various risks may cause Taysha’s actual results to differ materially from those stated or implied in such forward-looking statements. These risks include uncertainties related to the timing and results of clinical trials and preclinical studies of our drug candidates, our dependence upon strategic alliances and other third-party relationships, our ability to obtain patent protection for our discoveries, limitations imposed by patents owned or controlled by third parties and the requirements of substantial funding to conduct our research and development activities. For a list and description of the risks and uncertainties that we face, please see the reports we have filed with the Securities and Exchange Commission. This conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, May 11, 2021. Taysha undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call except as may be required by applicable securities laws. With that, I’d now like to turn the call over to our President, CEO and Founder, RA Session II.

Suyash Prasad: Thanks, RA. As RA mentioned, Taysha has a robust portfolio of 26 gene therapy product candidates for monogenic diseases of the CNS. Our candidates target broad therapeutic categories of immense unmet medical need, including neurodegenerative diseases, neurodevelopmental disorders and genetic epilepsies. We have recently added TSHA-120 for the treatment of giant axonal neuropathy or GAN to our pipeline, making it our most advanced program. We believe the preclinical and clinical data generated to date hold significant promise for GAN patients. Preclinical studies have demonstrated strong proof-of-concept data for both the construct and the delivery modality. TSHA-120 performed well in preclinical studies demonstrating improved motor function and nerve pathology and long-term safety across several animal models. Preclinical data also demonstrated that TSHA-120 showed a significant improvement in the pathological appearance of the dorsal root ganglia, a key component of disease progression. DRG inflammation is a topic that has been the focus of much discussion within gene therapy circles in recent months. This is because it has been observed as a histopathological finding in some non-human primate gene therapy studies, although the NHPs exhibited no functional compromise. Interestingly, in down and in the majority of diseases in our neurodegenerative franchise, the DRG have a significantly abnormal histological appearance and function as a consequence of underlying disease pathophysiology. Thus, it was not surprising that when treated with TSHA-120, we saw considerable improvements in the pathological appearance of the DRG in the GAN knockout mice. We are fortunate that in addition to robust preclinical results, those considerable natural history that provides us with patient data to identify optimal marcus and endpoints for a clinical trial. To date, there are data in 45 GAN patients that demonstrate an average 8-point decline per year in the MFM32 scores that are consistent across patients of all ages. Recall that the 4-point define per year in the MFM32 is considered clinically meaningful. Notably and in line with recently published FDA guidance, regulatory agencies appreciate the availability of a well-controlled and high-quality prospective natural history study as a comparator in clinical trials for rare diseases. In addition, we believe this natural history study provides us with a head start in identifying patients. Based on the positive preclinical results an R&D was opened, and TSHA-120 is being further evaluated in an ongoing clinical trial. The primary endpoint is to assess safety, with secondary endpoints measure of efficacy using pathologic, physiologic, functional and clinical markets. To date, 14 patients have been administered intrathecal TSHA-120 and six patients have at least three years worth of long-term follow up data. TSHA-120 has shown a dose-response relationship with the rest of disease progression at the second highest dose level, 1.8 times 10 to the 14 total VG at one-year post-treatment, affecting a statistically significant 8-point improvement on the MFM32 score, in comparison to the predicted natural history trajectory. These results are very promising as a full point change in the MFM32 score considered clinically meaningful. Six of these patients treated at therapeutic dose levels have shown sustained dose-dependent improvements in MFM32 scores for more than three years. Long-term results demonstrated that treatment with TSHA-120 at multiple dose levels was well tolerated with no severe drug-related adverse events. We look forward to reporting additional data later this year, including results from the highest dose cohort 3.5 times 10 to the 14 total VG. The FDA has already granted TSHA-120 orphan drug and rare pediatric disease designations, and we will continue to work closely with the regulatory authorities in the U.S. In the near-term, we expect to have discussions with the FDA and engage with other major regulatory agencies by year-end to discuss the pathway to approval for TSHA-120. I would also like to highlight some of the promising preclinical data coming from our earlier-stage candidates that demonstrate the incredible breadth, depth and velocity of our development engine. It is important to note that there are no approved disease-modifying therapies for any of the programs in our portfolio. With such compelling data to date for our pipeline, we are very encouraged as our gene therapy candidates could offer significant value to meaningful patient populations. We are very excited to show new preclinical data for TSHA-102 in Rett syndrome, that was recently published in brain. As RA discussed earlier, historically, it has been a challenge to find the right approach to safely regulate MECP2 expression in this disease. The complexities are highlighted by phenotypic variability, mosaicism and the need to regulate MECP2 such that it does not cause over-expression related toxicity. Today’s data give us confidence that we can achieve appropriate MECP2 expression in all cells in a genotype-dependent manner with no signs of toxicity. With the built-in regulatory element, miRARE, TSHA-102 provided a statistically significant survival extension in knockout Rett mice by 56%, while the unregulated mini MECP2 gene transfer failed to significantly extend knockout survival at either dose tested. Additionally, the unregulated full-length MECP2 construct did not demonstrate a significant extension in survival and was associated with unacceptable toxicity profile in wild-type mice. We believe that the 56% improvement in survival in TSHA-102 treated knockout mice is extremely impressive. I sees adolescent mice have accumulated significant disease. Of note, this Rett patients do not demonstrate symptoms until about one year of age, and therefore, will not be treated until after this point, we believe these data are likely to be highly translatable to the clinical setting. In addition to survival, behavioral side effects were explored, TSHA-102 treated wild-type mice have a significantly lower meaning better mean aggregate behavioral score than those treated with unregulated of full length MECP2 and then regulated mini MECP2. Importantly, miRARE mediated genotype dependent gene regulation or shown by analyze and tissue sections from wild-type and knockout mouse treated with AAV9 vectors given intrathecally. TSHA-102 demonstrated reduced levels of MECP2 in different regions of the brain, suggesting that miRARE inhibited mean expression in a genotype dependent manner. This demonstrates that TSHA-102 achieved MECP2 expression levels with the normal physiological parameters. In summary, these positive data demonstrated miRARE’s ability to exhibit genotype dependent regulation of MECP2 gene expression across different brain regions in both wild wild-type and knockout mouse models of Rett syndrome without overexpression toxicities. We are very encouraged by these results and look forward to filing an IND or CTA in the second half of this year, followed by initiation of a Phase 1/2 trial by year-end. TSHA-102 has the potential to address a significant unmet need for an estimated 25,000 patients with Rett syndrome across the United States and in Europe. Now I’d like to highlight some of our other preclinical programs that we have recently released data. TSHA-104, which is currently an IND/CCNA enabled studies for the treatment of SURF1-associated Leigh syndrome has demonstrated increased COX1 activity in brain and muscle and restored elevation of blood lactate on exhaustive exercise in a dose-dependent manner in SURF1 knockout mice. Dr. Qinglan Ling of UT Southwestern will be presenting these compelling data this Thursday at ASGCT. We remain on track to IND or CTA in the second half of this year. TSHA-105, our gene therapy candidate, which is currently in IND/CCNA enabled studies for the treatment of SLC13A5 deficiency caused a significant sustained decrease of plasma citrate levels up to three months post injection compared to aged mouse wild-type controls. TSHA-105 normalized EEG brain activity, reduced the number of seizures and reduced seizure susceptibility compared to vehicle-treated controls. Dr. Rachel Bailey will be presenting these positive data this Thursday at ASGCT. TSHA-103 is on gene therapy candidate that is an IND/CTA enabling studies for the treatment of SLC6A1 haploinsuffiency. And the SLC6A1 knockout mouse model, TSHA-103 improved nesting and EEG activity. In addition, in SLC6A1 knockout and heterozygous mouse models, TSHA-103 reduced spike train activity, which is a recording of abnormal neuronal activity associated with seizures. We believe the estimated prevalence is 17,000 patients in the U.S. and in EU. TSHA-111-LAFORIN and TSHA-111-MALIN, our gene therapy candidates in IND/CTA enabling studies for the treatment of both subtypes of Lafora disease achieved effective knockdown of GYS1 expression in the Lafora disease, LAFORIN and MALIN mouse models, respectively. Both product candidates decreased Lafora body formation within the brain and their respected mouse models. TSHA-112 has been tested in IND/CTA enabling studies for the treatment of adult polyglycosan body disease, or APBD. In preclinical studies, miRNA knockdown of GYS1-induced significant reductions in GYS1 mRNA, GYS1 protein, abnormal glycogen accumulation and polyglucosan bodies throughout the brain and an APBD knockout mouse model. For GM2 AB variant in preclinical studies, TSHA-119 caused a significant dose-dependent reduction of GM2 accumulation at 20 weeks in mice that were dosed intrathecally at Postnatal day one or at six weeks of age. Long-term follow-up, which include bi-monthly behavioral as well as biochemical and histological analyses are currently ongoing. TSHA-106 is being developed for the treatment of Angelman syndrome. In vitro testing and the neuro plus cell line demonstrated consistent knockdown of UBE3A-ATS and the subsequent increase in UBE3A expression across 26 distinct shRNA candidates. Selection of a development candidate is expected by midyear, followed by interim expression and safety data from confirmatory non-human primate studies by the year-end. TSHA-113, an AAV mediated gene knockdown construct has shown particular promise. TSHA-113 AAV9 capcid packages micro RNA shuffles are designed to target tau mRNA for all six isoforms founded the human and/or mouse brain. Treatment with TSHA-113 has shown a significant reduction in tau mRNA and protein levels while demonstrating widespread expression in neurons and GLIA. This is potentially significant implications for patients with neurodegenerative disorders characterized by deposition of abnormal tau protein in the brain, including Alzheimer’s disease, MACI associated frontotemporal dementia and progressive super nuclear policy. As you can see collectively, these preclinical data highlights our next wave of novel gene therapies, but for the potential to impact patient populations affected by significant diseases in a meaningful way. With that, we intend to file an IND/CTA for one of the following programs by the end of 2021. SLC13A5 deficiency, Lafora disease, APBD or GM2 AB variants. We also remain on track to file an IND/CTA and TSHA-102 in Rett syndrome and TSHA-104 and SURF1-associated Leigh Syndrome an IND with TSHA-101 in GM2 gangliosidosis in the U.S. during the second half of this year. We expect to initiate the Phase 1/2 trial for TSHA-118, which is under an already open IND. We are excited to have six near-term Phase 1/2 trial initiations planned throughout our portfolio. We are making incredible progress advancing our product candidates into clinical development, and we look forward to providing additional updates at our R&D Day that will span two days in June. We will continue to advance our pipeline by leveraging our next-generation platform technologies. As part of this initiative, we have recently established collaborations with Dr. Dennis Lal at the Genomics Institute, Cleveland Clinic, and Dr. Yang Xiaoyong at Yale University to further push the boundaries of AAV vector engineering by developing next-generation minigene Halos, this has the potential to overcome current limitations of packaging capacity, which is a critical barrier to treating genetic diseases not addressable for conventional AAV gene therapy technologies. This may enable us to effectively treat a wider range of devastating CNS diseases, UT Southwestern will produce bio vector constructs that incorporate the minigene payloads and evaluate the constructs in both in vitro and in vivo studies. Through collective efforts of Taysha and our partners, we will continue to strive for innovations and our platform technologies that will enable us to treat a broad range of CNS diseases with novel gene therapies. With that, I’ll turn the call over to Kamran to review our financial results.

Kamran Alam: Thank you, Suyash. This morning, I will discuss key aspects of our first quarter 2021 financial results. More details could be found in our Form 10-Q, which will be filed with the SEC shortly. As indicated in our press release today, R&D expenses were $23.9 million for the first quarter ended March 31, 2021, compared to $5.5 million for first quarter ended March 31, 2020. The increase was primarily related to the company’s development program as a result of increased manufacturing related spend, clinical and preclinical activity and headcount. G&A expenses were $8.2 million for the first quarter ended March 31, 2021 compared to $0.07 million for the first quarter ended March 31, 2020. The increase was primarily due to an increase in personnel costs, resulting from increased headcount, professional services fees, and other corporate related expenses. Net loss for the first quarter ended March 31, 2021 was $32 million or $0.87 per share as compared to a net loss of $5.4 million or $0.50 per share for the first quarter ended March 31, 2020. As of March 31, 2021, Taysha had $228.7 million in cash and cash and equivalents. We continue to expect that our working capital will be sufficient to fund our operation into 2023 inclusive of the development, regulatory and operational milestones RA and Suyash have outlined today. And with that, I will hand the call back to RA.

Operator: We’ll now begin the question-and-answer session. [Operator Instructions] The first question comes from Salveen Richter from Goldman Sachs. Please go ahead.

Salveen Richter: Good morning. Thanks for taking my questions. So one question here about – good morning. One question here about capital and resource allocation as you’re running multiple trials building out a GMP facility and hiring employees. So how should we think about that over time? And secondly, with regard to the Rett program, maybe if you could touch on the registration path here and what you’d like to see from that first clinical data set to inform the pivotal program.

Suyash Prasad: Absolutely. Thanks, RA and thanks for the question, Salveen. Yes. So for Rett syndrome, I think we’ve been spending a lot of time thinking about the clinical development program and the pathway to approval. And we’re going to take a slightly more cautious approach for some of our other conditions such as GM2, CLN1 GAN where the diseases are a little less common and where there is an ongoing relatively high-risk of mortality quite early on. So the way we think about Rett is that the first study of a group of two will be more of a Phase 1/2 primarily safety study with some exploration of preliminary efficacy. Following on from that, you will then perform a Phase 2/3 study, which focuses – it takes learnings from the initial Phase 1/2 study, take the learnings from that and applies it into a more expensive Phase 2/3 pivotal efficacy study. Now with regard to the first study, the Phase 1/2 study likely we’ll be do hit all older patients. As you know, FDA tends to push you away from children towards adults first and in this particular situation, we actually tend to agree with that approach. There are these risks of toxicity with over-expression of MECP2. So we just have to be quite mindful when we design this initial study. So the first study will be Phase 1/2 clinical pivotal safety, primary efficacy in the adult population in terms of endpoints will be looked at the safety aspects of safety initially. And then we’ll be looking at efficacy really in three different buckets. The efficacy will be looked at, firstly with a number of the different Rett-specific clinically rated scales, for example, the Rett syndrome motor behavior assessment, the Rett syndrome behavior question are. So they are the Rett scales, we’ll also be looking at seizures in some detail because children with Rett syndrome have significant seizure activity. So we’ll be looking at how frequent the seizures are, how many medications on, what triggers the seizures, how durable the seizures are and over time, hopefully will be able to see a reduction in seizure activity and bring them off medications and also see an improvement in the EEG. And then the third bucket kind of assessments will include a general multi systemic, multi-organ type aspects of Rett syndrome disease characteristics, such as the respiratory assessments, which, as you know, you have respiratory rhythm in Rett syndrome, sleep apnea issues, cardiac issues such as QT prolongation. So I think that the first, once again, will look at safety initially and some of these areas of preliminary efficacy, we will build on that and design the Phase 2/3 study subsequent to that. As we’ve already talked about, we’ll be engaging with regulatory agencies during the course of this year to pressure test our thinking around these particular plans, and we’ll be starting the clinical study towards the end of the year.

Salveen Richter: Thank you.

Operator: The next question comes from Matthew Harrison from Morgan Stanley. Please go ahead.

Unidentified Analyst: Good morning, this is Thomas on for Matthew. Can you give an update on where you are with manufacturing for the GAN program, in particular, what sort of assay work do you still need to complete? Thank you.

Fred Porter: Yes, thanks, RA. Thanks for the question, Matthew. Yes, obviously we’re in the process of onboarding the GAN program. And so where we’re really beginning is with the assays, reviewing the assays that were conducted by the NIH for the Phase 1, Phase 2 two clinical material, and what our intention is just try to update those methods to qualify and then validate them to prepare for a late-stage pivotal work. So, we’re actively engaging on all the critical quality attributes assays with our partners to move that forward with our CDMO. In addition, we’re looking very deeply into the potency assay development work, and this is something that’s happening, jointly between Suyash’s group and my own to move forward a potency assay very quickly to kind of synchronize a fully developed and qualified potency assay with pivotal lot manufacturing. I’m happy to answer any questions about that?

Operator: [Operator Instructions] Then one, the next question comes from Raju Prasad from William Blair. Please go ahead.

Raju Prasad: Hey guys, thanks for taking a question. Congrats on the progress. I’m kind of looking down your pipeline and I see a lot of the technologies that you’re de-risking from a payload perspective, the miRARE platform, the bicistronic vector, I could see follow-on indications once those technologies are derisked. But my question was more on the regulatory side. As you’re kind of dealing regulators on these different indications, what types of aspects of the programs do you think will be derisked by clinical data there? Is it on endpoints and deal with endpoints with the FDA? Is it on the IT administration? Maybe some color there would be great. Thanks.

Suyash Prasad: Thanks, RA and thanks Raju for the question. Yes, there’s lots and lots of commonalities, I think, between our programs, over and above the simple – the trifecta of comments we about AAV9, HEK239 and IT administration. There’s many, many other commonalities, I think we shared and we – as a platform more than anything. Let me touch on a couple of things – I think we’re going to learn a huge amount from just one program to inform the next. There’s a lot of debate in the field about IT versus ICM versus ICV and several contribution between them all. I keep coming back to the perspective that IT administration works has worked for decades. I’ve given it myself in the world of oncology and anaesthesiology and it’s worked for decades there. When you look at the clinical data from GAN from CLN3, CLN6, and another in Zolgensma, you see it works, and it works beautifully. And I think as we continue to build our portfolio of programs, we can really I think the FDA and other regulators will just become increasingly comfortable with intrathecal administration. And there’s many nuances around that, but many details. For example, we spent some time yesterday talking about a different type of think kits you might use to give intrathecal drug and the comparability – compatibility test you might need to do for some of these different methods of administration. So I think there’s lots and lots of learning, in particular from GAN that will inform the rest of our portfolio. Another piece of learning, I think that’s important from GAN and as our programs progress, just on the immunosuppression regime we like to use. So the whole world of the immunology of gene therapy has evolved and evolved rapidly over the past few years, initially, people didn’t get any immunological therapy and just treated liver inflammation reactively with oral prednisolone. When was decided that let’s give the prednisolone first to try and prevent it. And then additional medications have been rather than added. And we’ve settled very – on this very nice regime of six months of oral prednisolone plus 12 months of rapamycin and specific doses that we have a lot of experience with now and learnings from the GAN program, where a number of patients have been manage with this regime in expressive therapy very, very successfully. To the point actually, we’re not seeing any evidence of any T cell-mediated information in any of the patients who received this regime from the GAN study. We’re using that approach in GM2, in CLN1, in SURF1. And I think once again, we’re going to build up this body of evidence for that particular regime. I think the third thing I’ll mention, and you touched on it is endpoints in the clinical trial and what we can learn from one to other. I think for a lot of our diseases, where there are these neurological features. There’s a development called regression and a lack of failure to GAN milestones. And we’ve set on a very nice group of development to assessments the Bayley scale, the Vineland, the CHOP INTEND. And there’s one or two others that are more disease specific. We know how to train the rates that do these particular assessments. We know how to train the rates that do these particular assessments. We note of video, the assessments in a particular way, when it to upload the videos to a server, where they can then be reviewed externally by a second rater a second group of raters who are blinded to what the patients have been treated or not. All these things had a lot of robustness to the clinical development program and learnings from one to the other. The other thing I mentioned when we were talking about Rett a few minutes ago, was just seizures how we collect seizure information, seizure activity, EEG, the medications, the patients are on, et cetera. So I think that in our discussions with the regulators, there are many, many commonalities, in particular, on the clinical development side, but I think are going to be applicable to all programs and will constitute additional learnings from one to the other. I hope that answers your question, Raju.

Raju Prasad: Yes, that’s extremely helpful. Maybe just a quick follow-up on that last point. As it relates to the upcoming FDA discussions on the GAN program, how should we be looking at the results of those discussions as it relates to the potential request from the FDA. I’m thinking particularly about natural history comparator versus having to run a placebo arm or control treated arm. I mean is that something that you’re looking to see kind of as to extrapolate to the rest of the pipeline? Like if they do give you a natural history comparator for pivotal, that’s something that you might try for GM2 and some of the rare diseases? Or do you think that the discussions on GAN are only going to be related GAN and each individual indication will probably be a different – kind of a different kind of discussions with the agency. Thanks.

Suyash Prasad: So it’s a really important point. The – how much data are already existing for a particular disease. And it’s – there are certainly commonalities there from proven the program, but there are also some subtle differences, and we’re doing things a little bit differently from program to program. What I will say is a higher level is some very nice guidance that was published by the FDA on gene therapy development for neurodegenetive disease and have a specific section on natural history study in historical controls. They said very clearly, this may be appropriate for gene therapy product to treat a rare and serious neurodegenerative disease. If there’s a clear unmet medical need, which is absolutely the case for most of our programs, where the inclusion of current control is not practical or ethical, which is also true, certainly for programs like GM2 or CLN1, where there is ongoing higher risk of mortality. They also talk about the disease course is well documented. And the expected treatment effect is large, it may be very, very suitable to use a natural history comparator as a control. Now for GAN, specifically, we have 45 patients, in fact, more than that, we’ve presented data of 45 patients in the natural history study with data, that patients were enrollments in 2013. So it’s rates of [indiscernible] (0:47:23) data on some of these patients. And we’ve got very, very clear indication that there’s a consistent drop in the primary efficacy endpoint, the MFM32 8 points per year. I think because of that, it’s also predictable. The disease course is predictable. And so for GAN, very rare disease. With – and we’re seeing a very nice treatment effect in our international study. So all those things really contribute to the fact that for GAN, in particular, I think is – you don’t know what the FDA you’re going to say, but I think it checks all the boxes for a natural history study being an appropriate comparator. So my guess is it’s unlikely they will ask us to do any kind of more formal concurrent control. Once again, you don’t know at the FDA are going to say, but it checks all the boxes from that perspective. GM2, there’s a lot of already good natural history data out there in publications. And so we’re making use of that CLN1, there is a prospective natural history study ongoing currently with about 40 to 50 patients in it. This is international. So we’ll be using that. So it’s a little bit different from program to program. Rett syndrome, there is huge natural history databases that are available. Although for Rett, we will likely build in a concurrent control for a randomized, but non-blinded concurrent control. To add a little more robustness the clinical development plan. So let me start there. I hope I’ve answered your question and give us some context, but I can stop. I think we can go into more detail if you like, Raju, but most of that now.

Raju Prasad: No, that’s extremely helpful. Thank you for the question.

Operator: The next question comes from Eun Yang from Jefferies. Please go ahead.

Eun Yang: Thank you. Thank you. So today, when we talk about address the patient population for your gene therapy programs, it’s been kind of a focus on the U.S. and Europe. But now you look to potential approval of TSHA-120 in 2023, what are you thinking about the market opportunity outside the U.S. and Europe?

Eun Yang: Thank you. And I have one more question on Rett syndrome program. So I’m sure that you’re familiar with the Novartis program. And I don’t know how much you can speak about it, but aside from your program, potentially have a better regulation of the transgene expression. Can you talk about kind of a differentiation compared to Novartis, and Novartis actively pursuing their Rett program? Thank you.

Suyash Prasad: Yes. Thanks, RA, and thanks for the question. I think it’s an important question. As RA mentioned, the only – the major difference really is the fact that we include – we have the mini MECP2 gene, which was developed by Professor Sir Adrian Bird and very esteemed and ineligible Rett experts from Edinburgh who was actually first person to demonstrate unequivocally that Rett syndrome is a highly reversible disease. So we use his design for the mini MECP2 gene. And then we attach this strip of micro RNA binding sites, the miRARE platform, which stands for micro RNA a responsive of auto regulatory element. So when MECP2 levels go up within the sale as a consequence of the gene therapy, the down regulatory micro RNA binding sites are triggered, they bind to this miRARE platform, which is in the untranslated region of the construct and bring down levels of MECP2, as RA suggested, acting as a safety valve. Now we’re very excited to be able to say to you that the first quantitative data demonstrating this reduction in MECP2 expression to the point where you have enough so it’s efficacious, but not too much that is toxic, was published in brain, which is a very prestigious [indiscernible] (0:55:16). It went online on Friday, and we issued a press release yesterday. And I would encourage you to look at the paper, the lead author is Sara Sonet and senior authors are good friend and colleague, and our Chief Scientific Adviser, Steven Gray, there’s a particular diagram in that paper, which I’d suggest you look at, which looks specifically at different levels of expression of MECP2 in different parts of the brain in different parts of the spinal cord. And you can see very nicely that the non-miRARE construct over expresses whereas the miRARE construct expresses enough so that it is efficacious, but not toxic. So we’re very excited about that fixer paper. So I think that’s the main difference. The fact that we can demonstrate this – the ability to express MECP2 within these normal physiological parameters now we’ve shown in different parts of the brain, and we’ve shown it quantitatively as well. My understanding is that Novartis is still moving forward with that program. Last I heard was the planning to move forward as an IND, but I don’t know exactly where they are with that. But I think that’s the main difference really between our products unless.

Eun Yang: Thank you for the details.

Operator: There are no further questions. I will now turn the call over to Mr. Session for his closing remarks.

Operator: Ladies and gentlemen, this concludes today’s presentation. Thank you once again for your participation. You may now disconnect.