Good morning, and thank you so much for joining us today. I'm Kate Lang, Chief Commercial Officer at Avidity Biosciences. Today, we're excited to share the first functional data from the EXPLORE44 open-label extension study of delpacibart zotadirsen for boys and young men living with DMD exon 44. Before we get started, I would like to share that this presentation contains forward-looking statements as defined under applicable law. Forward-looking statements involve risks and uncertainties, both known and unknown, which may cause actual results to differ from the forward-looking statements contained in this presentation. You are cautioned to not take undue reliance on these forward-looking statements and to refer to the more detailed cautionary language in this slide and in the risk factor sections of our recent reports filed with the SEC. With that, I would like to hand it over to our CEO and President, Sarah Boyce. Thank you, Kat. Our vision at Avidity, as you know, is to profoundly improve people's lives by revolutionizing the delivery of RNA therapeutics. This morning, we're going to focus on DMD, and this morning, we're going to share with you how we're actually redefining what is possible in DMD. Joining me on the call today is my colleague, Stephen Hughes, our Chief Medical Officer, and I will have other colleagues join us for the Q&A portion of the meeting. At Avidity, we're now gearing up to launch three drugs, all in the same therapeutic space, in the neuromuscular space: delpacibart braxlosiran and delpacibart etedesiran. Delpacibart braxlosiran is for the treatment of FSHD. FSHD is a large rare disease. It was estimated to be about 45,000-87,000 patients, people living with FSHD in the U.S. and Europe, and we are on track to be the first ever globally approved drug for this disease. Etedesiran is for the treatment of myotonic dystrophy. Myotonic dystrophy is also a large rare disease with an estimated about 80,000 people living with myotonic dystrophy in the U.S. and Europe. And again, we're also on track to be the first ever globally approved drug for this disease, and a drug which clearly has a best-in-class profile for myotonic dystrophy. Now, moving to focus in specifically on DMD. As we all know, DMD is a devastating disease that affects young boys and young men and results in loss of ambulation, typically by the teenage years, and a significantly reduced life expectancy. It's estimated that for boys and young men amenable to exon 44 skipping, there's about 900 in the U.S. and about the same in Europe. What we're going to share with you today. Move back the slide, please. Slide clicker just stopped working. What we're going to share with you today is unprecedented data. What we're actually seeing is functional improvements, and that's improvements across all key measures demonstrated at one year, so this is for boys and young men who had enrolled in the EXPLORE44 study and gone on to the open-label extension study and are now out at 12 months of treatment. We're also going to share with you the compelling biomarker data of muscle health, and this is looking at creatine kinase. What you have seen before is the rapid, significant, and sustained reductions in creatine kinase. We're going to show you what this looks like out past 16 months, and this is the aspect of really when you can protect muscle fibers over the long term, what's possible, if you can get improvements. We're also going to share with you the continued favorable safety and tolerability profile, with most TEAEs being mild or moderate. We are, as a team, extraordinarily focused on making sure that we can get delpacibart zotadirsen to boys and young men living with DMD amenable to exon 44 skipping as quickly as possible. That route is through our BLA submission. We are on track to file our first BLA as a company. So this is the first of three in a 12-month period, but our first BLA as a company year-end of this year and launching in 2026. With that, I am now going to hand over to Steve, who's going to take you through the data. Steve, over to you. Thank you, Sarah. Okay, if we can move to the next slide, please. Today, I'm extremely excited and privileged to be sharing the functional endpoint data from delpacibart zotadirsen in the EXPLORE44 program in DMD amenable to exon 44 skipping. But first, I'd like to take a few moments to remind you of the study design and the biomarker data, and then, as always, the safety data from the EXPLORE-OLE study. The first study, EXPLORE44, is on the left of the slide. It was randomized, double-blinded, and placebo-controlled, and involved 26 boys and young men with DMD exon 44, 19 on delpacibart zotadirsen, and 7 on placebo. All participants received three doses of either placebo or delpacibart zotadirsen at 5 mg/kg or 10 mg/kg. Muscle biopsy was performed one month after the last dose, and participants then had the opportunity to roll into the open-label extension, which is in the center of the slide. Here, they all received delpacibart zotadirsen. Participants initially rolled over on either 5 mg/kg or 10 mg/kg, depending on what dose they were on in the parent study. You'll recall that at the end of last year, we agreed with FDA that 5 mg/kg every six weeks would be our go-forward dose for potential accelerated approval. Since then, all participants in the OLE have moved to their dose regimen. We've also enrolled an additional 16 participants with DMD exon 44 in the open-label extension to bring the overall safety database up to 39. These new participants are purely contributing to safety. They're not having muscle biopsies because we've already aligned with FDA that the dystrophin data we have is sufficient for BLA filing. So in total, we have 39 boys and young men with DMD-44 that have received delpacibart zotadirsen. These span a broad age range from seven to 27, both ambulatory and non-ambulatory, and also a range of different mutations, and most are receiving corticosteroids. Functional data we'll be sharing today comes from the one-year time point in participants that have had at least one year of continuous treatment with delpacibart zotadirsen at either five or 10 mg/kg. So they've completed the EXPLORE44 study and have several months of follow-up in the open-label extension study. Safety data, as always, comes from all participants, including the 16 new participants. Next slide, please. You'll recall that we shared the top-line safety data from EXPLORE44 earlier this year. At that time, all of the boys had already finished EXPLORE44 and rolled into the OLE. So there's no new data from the EXPLORE44 to share today. So the data we are sharing is an update from the OLE with a very recent data cut of June of this year. The long-term safety of delpacibart zotadirsen continues to be extremely favorable. 39 patients enrolled in the OLE, including 23 that rolled over from EXPLORE44 and the 16 new participants. Most adverse events have been mild or moderate. The most common AEs, i.e., those occurring in greater than three participants, are those that are frequently seen in any clinical trial, even in placebo arms. There have only been three participants that experienced a serious adverse event, and only one of these, which was a moderate hypersensitivity, was deemed to be related. Two unrelated serious adverse events were a fractured femur and a suicide attempt. Hypersensitivity was not atypical in any way and was not associated with changes in vital signs or oxygen saturation, but did result in the patient being withdrawn from the study. Next slide, please. Before moving to dystrophin expression, I'd like to just remind you of a couple of important nuances. Not all dystrophins are created equal. The dystrophin gene, shown at the top of the slide, is one of the largest in the genome, with 79 exons, and it codes for a large protein with many different domains, which have important functions in terms of muscle health and function. The dystrophin that we make by skipping exon 44, as you can see in the middle of the slide, is a near full-length dystrophin and, as such, retains the functionality of the protein. In contrast, and as we can see at the bottom, the microdystrophin made by gene therapies is only about 30% of full-length dystrophin protein and therefore sacrifices several of dystrophin's functional domains. Next slide, please. On the left is the dystrophin data that we shared with you back in March, and it's very clear that del-zota is producing unprecedented levels of near full-length dystrophin. At both the five and 10 mg/kg doses, we get around a 25% increase in dystrophin levels, which takes these boys, on average, to dystrophin levels of over 30% of normal. To put this into context, female carriers of DMD have about 50% of normal dystrophin and typically are asymptomatic. With del-zota treatment, we're approaching levels of dystrophin that are associated with a normal phenotype. Of note, we have not adjusted this data for muscle content. These are just the values from the Western blot, normalized to myosin heavy chain. The right side is showing new data. Here we see the percent positive dystrophin fibers on muscle before and one month after three doses of delpacibart zotadirsen for a representative patient. Not surprisingly, given the very large increases in dystrophin on the Western blot, the increases in dystrophin-positive fibers are very clear to see. Also, you'll notice that the fluorescence is around the muscle cell membrane, indicating that the dystrophin is correctly localized within the muscle. We've already seen earlier this year that this high level of dystrophin production resulted in near normalization of multiple markers of muscle health, including CK, myoglobin, ALT, and AST, showing for the first time in DMD that delpacibart zotadirsen is protecting muscle fibers from damage. In the next slide, we'll see how the large reductions in CK that we observed are holding up over the long term. Next slide, please. I think the conclusion is that they're holding up very well. Here we see that out through 16 months of treatment, we're maintaining near normal CK levels. And because CK is a biomarker for muscle damage, this confirms that delpacibart zotadirsen continues to provide long-term protection from further muscle damage. Notably, at the one-year time point, about 50% of participants had CK levels within the normal range. In a moment, I'm going to show you how this long-term protection is translating into improvements in functional measures. And in order to put these improvements into context, we've compared with matched patients from the PRO-DMD-01 natural history study. Next slide, please. I would like to draw your attention to the right of the slide. PRO-DMD-01 is a prospective natural history study following 269 boys and young men with genetically confirmed DMD. In order to ensure as much of an apples-to-apples comparison as possible, we selected participants from natural history to match as closely as we could for those in the EXPLORE44 OLE. We were able to match 22 natural history participants based on being DMD 44 skip amenable, age seven to 27, on steroid treatment and a stable dose for at least a month, and body weight greater than 23 kilograms. On the left of the slide are the baseline characteristics for the key assessments. These tell us a few things. Time to Rise from floor reaches about five to seven seconds, ambulation declines meaningfully over a one-year period. Based on the high value of the Time to Rise and other ambulatory measures at baseline, these boys will be expected to decline significantly over the one-year period. Secondly, although generally well matched, the participants in the EXPLORE44 arm are worse on all measures at baseline and therefore will be expected to decline more quickly than the natural history group. This is important because it makes the data I'm about to show you even more remarkable. Finally, the assessments on this slide are all measures of ambulation. These assessments are all in ambulatory patients only. Out of the 17 participants in EXPLORE44 that had reached the one-year time point, 12 were ambulatory, but one had a fractured femur and another had sprained his ankle. Therefore, 10 participants in total are included in these assessments of ambulation. We've also looked at the pool in both ambulatory and non-ambulatory patients to assess upper limb function, and I'll show you this a little bit later. And remember, we've pooled the five and 10 mg/kg patients for all of these analyses since the amount of dystrophin restoration and CK reduction was essentially the same at both doses. And now what you've all been waiting for. I'm extremely excited to show you how this long-term protection from muscle fiber damage is translating into improvements in functional endpoints. Next slide, please. On all of the functional endpoint slides I'll show you, the zero on the figure represents baseline. Moving to the left is a reduction from baseline or worsening of disease, and movements to the right are improvement. Here we see the Four-Stair Climb. And I think it's very clear to see that delpacibart zotadirsen-treated patients are showing an absolute improvement of greater than two seconds, whereas natural history, as expected, are declining quite a bit by greater than two seconds. So relative to the natural history, delpacibart zotadirsen is leading to close to a five-second improvement. This has never been seen before. And remember that to do this test, boys not only need to be able to walk, they need enough strength to be able to climb upstairs. Next slide, please. Now the 10-Meter Walk/Run Test. And here again, we see absolute improvement in the delpacibart zotadirsen-treated boys compared to declines in natural history. And compared to natural history, the delpacibart zotadirsen-treated boys are improving by around two seconds. Next slide, please. Here Time to Rise from floor is a complex test. Although the boys were still ambulatory, not all boys were able to get up from the floor. So we only have data on six for delpacibart zotadirsen and 19 for natural history on this assessment. Consistent with the other measures of ambulation, substantial absolute improvements in the delpacibart zotadirsen-treated boys are seen compared to a decline in natural history, with an overall nearly five-second improvement with delpacibart zotadirsen compared to natural history. Again, improvements that have never been seen before. Next slide, please. The North Star Ambulatory Assessment is the last of the ambulatory measures. Here, we only had data on 20 boys from natural history. Again, we see improvements relative to natural history, with an overall improvement of about 2.5 seconds. So we're seeing very consistent and, quite honestly, quite unprecedented improvements in all of these functional measures. Now we'll look at upper limb function. Next slide, please. Here we're looking at the Performance of Upper Limb 2.0 tests, and the results shown are for the pooled ambulatory and non-ambulatory patients. Although when we look at them individually, there's no difference between the non-ambulatory and the ambulatory for the improvements. The pool is not included in the PRO-DMD-01 natural history study. For this comparison, we've used the published literature for a comparison, and the citation is at the bottom of the slide. There are 27 exon 44 skip amenable boys from natural history and 17 treated with delpacibart zotadirsen. We can see that consistent with the ambulatory measures, upper limb function is also improved for delpacibart zotadirsen boys. In comparison with natural history, this improvement is over two points. Next slide, please. Finally, an overall summary of what we shared today. As we can see on the right of the slide, we see consistent and clinically meaningful improvements across multiple functional endpoints, assessing both upper limb and lower limb function at one year. We've seen large and statistically significant dystrophin increases, delivering sustained improvement in CK and long-term protection of muscle from contraction-induced muscle damage. We've also seen very favorable long-term safety and tolerability. So for the first time, we've been able to show that large improvements in near full-length functional dystrophin are associated with sustained long-term muscle protection with subsequent reversal of disease progression as compared to natural history. I'll now hand back to Sarah for closing remarks. Thank you, Steve. Go to the next slide, please. What we've shown you today is really part of this ongoing revolution that we're leading in what's possible in RNA delivery. Redefining what can be possible for boys and young men living with DMD. What we've seen is unprecedented functional improvements, which is essentially reversal of disease progression. Boys and young men amenable to exon 44 skipping. That's a big statement to be able to say for DMD. You also see the compelling biomarker data of muscle health. When you can get the unprecedented levels of dystrophin that we were able to achieve, creatine kinase and the other markers of muscle health go down, stay down. And when they do that, you can actually get people doing more. All of this is at the favorable safety and long-term tolerability profile. We are 100% focused on the importance of the jobs that we need to do in getting delpacibart zotadirsen to this community as quickly as possible. That's part of our commercial readiness. We're finalizing our confirmatory Phase 3 study design with regards to bringing delpacibart zotadirsen to boys and young men around the world. We are on track to submit our first BLA as a company by year-end. The functional data clearly further reinforces the potential for accelerated approval, as well as also the work that we're doing to prepare the global development pathway. Essentially, part of this is often boys living with DMD and young men living with DMD are referred to as DMD boys. Our goal is where they just become boys. And that's doing things like jumping on sofas, skipping, being able to reach up and get stuff, being able to game, and really looking at redefining what's possible for DMD. We're now going to move into the Q&A portion. I'm going to have Steve join us back on screen, Michael Flanagan, our Chief Scientific Officer, who I know you all know well, as well as Kate Lange, our Chief Commercial Officer, who you all know. Also join us back on screen, and we'll move to questions. All right. Thank you, everyone. We've got a number of questions coming in here on the portal. I'm going to go ahead and take through a few of those. Our first question comes from Eric Schmidt and Josh Schimmer. It's great to see patients on delpacibart zotadirsen gaining function as opposed to a reduction in rate of decline. So we have a two-part question here. The first part from Mike. How do you think about the biology underlying this observation? Yeah. So I think, once again, we've connected the dots, right, from delivery, where we see unprecedented delivery, to production of dystrophin. That dystrophin being nearly full length is really important. And that leads to these sustained and significant decreases in CK, which gives you that muscle protection. And then what you saw today was from Steve looking at the long-term functional improvements that we're seeing. So again, it's that connection from the delivery, our ability to now deliver RNA to muscle, and we've shown that across three different programs, to that effect on the target, to the effect of the downstream biology, and then that biology turning into functional improvement. So it's really, I mean, you don't see this that often. It's pretty exciting. Excellent. And then the second part of the question for Steve, should we expect gains to continue over time? Yeah. We're not seeing any reason why these gains can't continue to improve. I mean, the real thing here is just providing the long-term protection from further contraction-induced muscle fiber damage. And we're seeing already that through 16 months, these boys are down near or within the normal range, reflecting that long-term protection. So as the protection stays out through the long term, we would anticipate that we would see further improvements in muscle strength and function going out over time. Great. Thank you. And then our second question comes from Joseph Schwartz at Leerink. Joseph, congratulations on the data. Thank you, Joseph. The question goes to Steve. Is the methodology for the natural history control arm consistent with how the FDA would like it done in a propensity matched or weighted manner? Yeah. So as you can imagine, we extracted 22 participants that we were able to match for the comparison. DMD 44 is only about 6%-7% of the total. Within that natural history study, there are actually only about 27 or 28 DMD 44 participants. Really hard to do things like propensity matching. We just have to work with the tools that we got. But they were well matched at baseline for important characteristics from our eligibility criteria. We saw on the baseline characteristic slide that they were pretty much similar in age. And that on all of the functional measures at baseline, actually, the delpacibart zotadirsen-treated participants were worse at baseline than the natural history patients, which means that the delpacibart zotadirsen patients would be anticipated to progress even more than the natural history over that one-year period in the absence of treatment. So any biases that are inherent in the results actually bias in favor of the natural history, not in favor of delpacibart zotadirsen. Great. Thank you. Our next question comes from Geoff Meacham at Citi. This one goes to Sarah. So Sarah, you're planning to start three BLAs over the next 12 months, beginning with delpacibart zotadirsen by year-end 2025. Could you comment on how these successive launches could build upon each other in terms of awareness of Avidity AOC products and the commercial infrastructure of a rare disease launch? Yeah. Thanks, Geoff. And good to see you covering us again. So in terms of from an aspect, one of the most important elements to understand here is that each launch is synergistic with the other because this is in the same therapeutic space, so in the neuromuscular space. In the case of FSHD and myotonic dystrophy, essentially, there is 100% overlap in the potential prescribing physicians. So what we're able to build is a very efficient commercial organization, obviously starting with delpacibart zotadirsen and DMD, where there's also the pediatric neuromuscular specialists. We are very far along on that. We have our MSL team in place. We have our patient services organization now building all of the infrastructure that will be required. We have a site-of-care team in place. We have a payer team that is already on the ground in the U.S., as well as also having a marketing team and a market access team also in place. So a big part of all the infrastructure of the commercial organization is already up and running. And a big element of this, when you look at what we're doing, is really unprecedented from an aspect of these are three successive launches all with the same commercial organization and all in the same therapeutic space. It's all in the neuromuscular space. I think suffice to say, in the neuromuscular world, people are going to know us pretty darn well from an aspect of being able to deliver three drugs to this community that really make a profound impact on people's lives. Excellent. Thank you. Our next question comes from Ritu Baral at Cowen. This one goes to you as well, Sarah. Has there been any meaningful reviewer turnover in your CDER neurodivision at FDA? Great question, Ritu. The answer to that is no. One of the other aspects of the synergy from one program to another is they're all reviewed within Neuro Division 1. There's a lot of the same people across the different review teams. We've worked with them for a long time now across all three of our programs. We speak, as you would expect, very often. The team has remained in place. It's all consistent. They are very thoughtful and helpful with their input, they're timely with their feedback, and really are focused on doing their job around also getting drugs to patients. So we are very grateful for the collaboration that we have with the division and with all the work that we're doing with them. And we have a second part to the same question from Ritu. So Sarah, given the strength of the functional data, will you approach Europe about approval? It's a great question, Ritu. As we've known with regards to for dystrophin, there is not an accelerated approval pathway in Europe. We did actually, on the data that we'd already seen back last year with dystrophin, we did go and have a conversation with EMA about the possibility for some sort of conditional approval in Europe just based on the dystrophin. The answer was no, and that we would need to show functional data. So that's where we're now in the process of locking down our global confirmatory study design. And it would be our expectation that that would be required. We are also a team that always believes in going back and having another conversation. And we will also we do also plan to do that with EMA based on the data that we've seen. But I would say our expectation is that the global confirmatory study will be required. Great. Thank you. Our next question comes from Yanan Zhu at Wells Fargo. Steve, we have a two-part here for you. I'll start with part one. Congrats on the data. Could you describe the bar of a clinically meaningful difference for each of the functional endpoints reported? Yeah. So the clinically meaningful important differences for this disease, as we look through the literature, have really been calculated based upon standard deviation or standard error or fractions of those. So we didn't include the MCIDs on the slide because the regulators really like for these differences to be calculated using anchor-based methods. In other words, by showing correlations with patient-reported outcomes where the differences are known. For Time to Rise, based on the literature, around three and a half seconds. Four-stair climb around two seconds. 10-meter walk time around two seconds are what we found in the literature for the MCIDs for these. So we've exceeded on all of the measures, the MCID as compared to natural history. Star two-point change is taken to be a clinically meaningful change. So there we also will be. One would be beyond the clinically meaningful difference that we could find in the literature. Great. And then the second part of the question, do you expect the NSAA endpoint to show improvements on baseline with longer-term follow-up? Yeah. Certainly, we anticipate that the ambulatory measures and upper limb function will continue to improve over time. The problem with the North Star ambulatory assessment, and this has been reported widely in the literature, is sensitivity. So at baseline, the average North Star score for the delpacibart zotadirsen-treated patients was 19. The maximum score you can get is 34. It's a 17-point scale. And patients score from zero, i.e., they can't perform the test, or either a one or a two. And a two is essentially normal. So with a score at baseline of 19, it means that on pretty much every single assessment, the delpacibart zotadirsen-treated participants were scoring a one. So in order to show improvement on that test, they have to basically go back to normal. Now, that may well be possible over time, and we certainly hope that they can do that. But in a one-year timeframe, that's just really difficult to see on the North Star. And we're not the only sponsor that's bumped up against this lack of sensitivity for that test in these shorter-duration studies. Great. And our next question comes from Gena Wang at Barclays. This is Steve. This is one for you. Can you elaborate on the SAE of hypersensitivity related to study drug? When was the onset? How long did it last? And how was it resolved? Yeah. So this was a classical infusion-type reaction. It occurred during the infusion. It was actually the third infusion for this participant. It occurred a few minutes into the infusion. It was moderate in severity. There were no atypical features. There was no difficulty breathing. There was no tissue swelling. There were no changes in blood pressure. There were no changes in oxygen saturation. The infusion was stopped, and the patient made a full recovery within a few minutes of stopping the infusion. They were treated with some Benadryl. They didn't require any admission to hospital. They went home, and there were no long-term sequelae. It's unfortunate that the participant was discontinued from the study, but really, this was just a typical reaction that you could see with biologic drugs sometimes. Thank you, and then our next question comes from Keay Nakae at Chardan. Mike, this one's for you. What is the read across of this data to your other DMD programs, such as DMD 45? Yeah, so for DMD 45, as you know, is our next an IND enabling, so that'll be coming toward the clinic in the near future. The other exons we're working on them in the lab currently. We have really good sequences, the PMOs we've selected, and those will be moving forward. We're really looking at also platform designation to look at those moving forward, and just to give you a sense of what we're anticipating for these is that given what we've seen to date for 44, we anticipate that the other exons will also perform really well, and when asked about this, we don't know exactly what it is. But even if we saw a third as much dystrophin production, that would be still well north of 10% expression of dystrophin, which I think puts you in that category where it's maybe not a normalization like we're seeing for 44, but it clearly puts you in the Becker's range. So for our exons that we're moving forward in the future, we're really looking to make that profound improvement in patients' lives. And we believe that that is producing dystrophin at a 10% level or above. And that's what we've done today. Thank you. And then our next question comes from Corinne Jenkins at Goldman Sachs. Steve, can you provide more detail on the process and timelines for receiving platform designation and how that could enable faster development timelines across a broader DMD population? Yeah, that's a great question. In order to get platform designation, one of the drugs in the platform has to be approved by FDA. The timing for us applying for the platform designation is after we actually get the BLA for del-zota. We will be submitting that application as soon as possible because, as you know, it is incredibly important for the development of our subsequent exons. Once you have platform designation, there are a number of potential ways in which it can accelerate the development path. First, on the CMC side, you can leverage your prior CMC work with your other exon skippers to reduce the regulatory burden of submission for your IND and also subsequent regulatory submissions. On the tox side, you can leverage your prior toxicology studies to start your clinical trial. That allows you to move to start clinical trials more quickly. And then within the clinical trial itself, you can start certainly at higher doses than you have to for your very first drug and ideally start even at your target dose. So that really reduces the burden on the clinical trial. And then at the time of application for BLA, then you can leverage your prior safety database. So that potentially reduces the number of participants that you need to have in your clinical trials for subsequent drugs in order to file for a BLA. So multiple, multiple different efficiencies there that we would be looking to exploit as we move the other exons forward. Great. Thank you, Steve. And then we're actually coming up to our last question here. This one goes to Mike. Can you discuss the impact of delpacibart zotadirsen on CK levels in non-ambulatory DMD 44 patients? Yeah. As you can see from the data, and again, it kind of comes back to that connecting the dots, it's that you see rapid and sustained improvements in CK. And that's across ambulatory as well as non-ambulatory. And you can see that the error bars are really small. And 50% of patients, and that includes both ambulatory as well as non-ambulatory, are in the normal range. That's unprecedented. That's really muscle protection occurring because we're making so much dystrophin. And that's leading to those functional improvements. And for the ambulatory boys, like a 10-year-old boy, once they're starting to feel better, you are not keeping them down, right? They're going to be running around. So that is a sustained level. It's not that you're seeing like, "Oh, they're running around and starting to use their muscles more," that you see a bump in CK. It actually stays down. That really leads back to the delivery, the expression of dystrophin, the effect on CK, and the functional benefit. And you're just seeing a completely different story than you've ever heard before of the effect of dystrophin and the long-term effect on muscle protection leading to this dramatic improvement. I think it's just you don't get to see this very often. So it's exciting. Thank you, Mike. And that concludes the Q&A portion of our webcast. I will turn it back over to Sarah for closing remarks. Thank you, Kat. And thank you, Mike and Steve, for joining us for the Q&A. Thank you, everyone, for joining us this morning. And I hope we have once again shown you how we're delivering on our vision to profoundly improve people's lives by revolutionizing the delivery of RNA therapeutics. And today, we have essentially redefined what is possible in DMD. Thank you.