... I think we're, we're ready to get started. Welcome, everyone. I'm Josh Schimmer from the Cantor Biotech Equity Research Team. Very pleased to introduce Ryan Watts, Chief Executive Officer of Denali Therapeutics. Ryan, welcome. Yeah, great to be here. You got a lot going on, but I think the most pressing update for the portfolio is gonna be the tividenofusp alfa PDUFA date coming up ahead. So if you would give us a quick snapshot of where Denali is in prosecuting- Yeah- the portfolio. I'd love to. I'll give just a quick introduction to Denali and then talk about Tivi. We just shorten it to Tivi. It's a lot easier, but. Thank you. Yeah, so, you know, obviously, a decade ago, when we founded Denali, our goal was to engineer brain delivery, and at the time, we were working on both small molecules and large molecules, and just starting really de novo to invent a blood-brain barrier technology. And I feel it, like a decade later, you know, there's a large number of companies working on transferrin receptor-enabled technologies, CD98, other blood-brain barrier technologies. And what we did in the first five years was to invent the transport vehicle, the next five years, prove that it works, and by proving it works is submitting our first BLA, and that is for Tivi. Just a little bit of background on Tivi. It's an enzyme replacement therapy that's fused to an Fc, and that Fc binds to transferrin receptor so that it can readily cross the blood-brain barrier. One of the things we've learned about transferrin receptor is it also enables great tissue penetration, for example, in the muscle and the bone. And so as we started, you know, these Hunter syndrome trials and now Sanfilippo trials and others, what we see is great distribution throughout the body, the whole body, in addition to the brain. And so we filed the BLA several months ago. I think for us, it was, you know, it's an interesting time to file a BLA working with the FDA, and we saw within, you know, the sixty-day window, we got a priority review and a PDUFA date of January 5th. And since that point, we've had a lot of interaction, including the, you know, Day 74 letter, and more recently, the Mid-cycle review and a lot of progress. And so that's been, I think, important for really the first transport vehicle-enabled molecule blazing the trail for the rest of our portfolio, and I'm sure we're gonna get into our other programs, but, it's an exciting time at Denali. Let's talk about the MPS IIIA program because that you gave us a development path and strategy there that postdates new FDA leadership. Right. So that can be another insight into how the FDA is thinking about biomarkers. So maybe share what happened there and to the extent you think that helps further reinforce Tivi's regulatory prospects. I think, the way you articulate the question is exactly right. I mean, for us, it was, could we hit repeat on what we're doing in Hunter, in Sanfilippo, but find a way to do it at roughly half the cost, and ideally, roughly half the time? It's a MPS disease, same biomarker, heparan sulfate. We're measuring it in cerebrospinal fluid, which is representative of the concentration of heparan sulfate in the brain. Basically, this program was selected for START, which is a continuous engagement with the FDA. We meet with them quarterly. The first topic that we really addressed with the FDA is the design of the confirmatory phase III trial. In fact, I should just note that just today, there's been more guidance provided by the FDA, both CDER and CBER, on rare disease, on evidence principles, in particular around single-arm trials. That's actually kind of interesting guidance because this guidance really focus on populations less than a thousand patients in the U.S., which is both Hunter syndrome and Sanfilippo, and discusses this idea of single-arm studies, which is pretty consistent with our programs, including the Sanfilippo program. The conversation began, you know, let's imagine four years ago, when we're designing the COMPASS trial, we asked the FDA if we could do a natural history comparator, and the answer there was actually no.COMPASS is now a, you know, it's actually comparing to standard of care to Elaprase, but it's different for Sanfilippo, and it's likely that we'll use natural history as a comparator for that particular study. That was topic number one. We needed a general agreement on where we were going there before the FDA... We engaged the FDA on the accelerated approval package, and there we got agreement on AA using heparan sulfate. Remember, this is a single enzyme disease, monogenic disease. 20 patients, we're just about done enrolling that phase 1/2, and then it's a 49 week endpoint. So basically, it's about. It's actually less than half the size of the phase 1/2 for Hunter. But I think the way that you ask the question is right. This is further evidence that the FDA wants to accelerate and wants to engage in rare disease drug development. I think today's guidance, which is really like brand new, is consistent with the experiences we've been having with CDER and with the FDA. Assuming everything goes smoothly, you'll be launching Tivi in 2026, and it's probably gonna be almost everything anyone cares about over the course of the year. Why don't we start talking about the commercial dynamics here, maybe just starting with the patient population, how many Hunter patients in the U.S., and as we think about their segmentation, neuronopathic, you know, who is your key target audience? Yeah. So I think hopefully, we can get proficient at answering these questions, so we can talk about everything else that's in the portfolio, but they're very important questions, so roughly 400-500 patients in the U.S. 2,000 worldwide. And if you think about the split at diagnosis genetically, it's actually hard to know if a patient will be neuronopathic or non-neuronopathic. But if it's a severe mutation, it's highly likely that they're neuronopathic, and that represents roughly 70% of newly diagnosed Hunter patients. Obviously, the attenuated patients live longer than the neuronopathic. Even on standard of care, neuronopathic is still, you know, you're looking at mid-teens as an average lifespan with neuronopathic, so that's generally the epidemiology of Hunter. The vast majority of these patients are on Elaprase. Even the neuronopathic, which don't benefit from a CNS perspective, they're on Elaprase to treat peripheral disease, you know, liver, lung, hearing, other, cardiovascular issues. So maybe we can talk a little bit about the infusion time, 'cause when we talk to specialists, it does seem to matter for some families who don't necessarily want to stick around for hours of an infusion. And as we think about that spectrum of disease, how are you thinking about... And maybe you can help characterize the infusion time- Right ... versus Elaprase, and for whom is it gonna be an attractive switch to say, "You know what? I'm gonna spend more time every week infusing because I feel like these benefits on the CNS, component are gonna be meaningful? Yeah. So the infusion time of Elaprase on, by label is three hours, and with the ability to accelerate as you build tolerance. So as the case with all enzyme replacement therapies, there is infusion-related reactions, as it's recognized obviously as a foreign protein. But as you dose weekly, over time you build tolerance. We see that with Tivi as well. Our average infusion time is approximately four hours, and in both cases, both with Elaprase but also with Tivi, as you build tolerance, you can accelerate that infusion time. What's been a game changer for us is that the infusions start in the clinic, but then over time, you go to at-home infusions. And I think what's been most interesting is these at-home infusions, we can also do them, like for example, with a backpack. So these young boys, which is the vast majority of Hunter patients, can run around, and they can be wearing a backpack as they have these infusions, right? So we're focused ultimately on at-home delivery, and that's gonna be I think the key point, is that you have a nurse team that comes to your home, and then, you know, most of the activities of daily living can go as planned. And in fact, we were just at a family conference, and I was meeting with the father of our very first patient and talking a little bit about his experience, and this is exact. He said, "Oh, yeah, we put the backpack on him, and then he runs around in the yard for the day," 'cause we're, you know, just trying to understand that. So that will be the goal. I think initially you start in the clinic. As you build tolerance, then you shift to at-home dosing. But 3 hours for Elaprase, 4 hours for Tivi, and then, of course, if you look at the label for Elaprase, you can go as fast, but not faster than 1 hour. And part of it is the first 15 minutes is slower, and then if you think about Tivi is 15 mg per kg, Elaprase is 0.5 mg per kg. But at a molarity level, our dose is 15 times larger. So even at the infusion rates that we're going, we're still delivering a lot more enzyme than Elaprase in that 4-hour period. Will, will you be sharing more granularity around the percent of patients that can get to shorter infusion times? So when- Yeah, I actually don't have that data, and I think it will depend obviously on the tolerability. But if you look at our tolerability profile, you see that IRRs dramatically diminish over time. So I think there will be a chance to accelerate across most patients. I think Elaprase is now priced at around $500,000 a year, maybe not as expensive as some of the new ultra-rare orphan drugs that have been approved. Do you see room for premium pricing even above Elaprase, and how do you think about capturing the full value of Tivi? Yeah. So I think the really important for us is broad access, and so we have to price thinking about access. We have to think about both the neuronopathic and then, more broadly, the, what we would call the attenuated population. When you think about these two populations, they're actually a, it's a continuum. Even attenuated patients have, you know, neurological symptoms ultimately. But the goal is we don't want to price so that the thought is, well, this is really a neuronopathic-only medicine, right? And so I think access is important. That being said, it... You know, the data, and especially when all the vast majority of our data is switching from Elaprase, you see superiority on biomarkers and on clinical data there, I think warrants premium pricing. Okay, got it. And then how are we thinking about cost of goods? Because you're at a much higher dose than Elaprase, but I think on the other hand, you've talked about some manufacturing efficiencies- Yeah ... that may benefit. Yeah. So I think historically, enzymes for enzyme replacement therapy are actually pretty difficult to manufacture, and in part because you have no real tag for purification. You take a natural enzyme, you purify and then you have to purify it through multiple columns. All of our TIVI-enabled programs use Fc fusions, and the Fc fusion allows two things. Number one, it actually provides better stability for the overall construct. So often, when you have a difficult-to-express protein, you make it as an Fc fusion, and it expresses much better. So our expression levels are much higher across the cell, you know, our stable cell lines. Number two, you use a Protein A column for purification, so this ends up being much more like standard biologics. So we expect our COGS to be in that range of about 20%, you know, when you think about that, and it's really based on the manufacturing. And we will drive that down over time. Again, cell lines being able to produce more and using Protein A columns, so it's a much less complicated purification for these ETVs. It is a small patient population to begin with. If we start segmenting into, you know, those who may stick with Elaprase, those who might take a gene therapy option, we may see JCR enter the market in the next couple of years with, with a different profile, you know, shorter infusion time, but not the strength of efficacy that you've demonstrated. How are you thinking about market, market share, and ultimately building a reasonably profitable franchise here? Yeah ... as what, I'm guessing you're envisioning as a tip of the spear for the broader portfolio? Yeah, yeah. Yeah. I mean, there are two ways to look at it. One is the exact details around the Hunter launch itself and the different patient populations, and switching is definitely a focus of our field team, of which, by the way, are hired and ready to go. The other is that this is just the beginning of a broader franchise, and so the patient experience and our patient service is gonna be so important for Hunter because the same physicians will treat Sanfilippo and will treat Pompe, although that's a much broader population. And so the goal here is to gain that momentum across all of these franchises. And part of it is, you know, something that's easy to express and purify, reasonable COGS, robust efficacy, flexibility on dosing. I think those are all key aspects here. But you're right. I mean, I think there are gonna be those that are eagerly awaiting for gene therapy in particular, especially the gene therapy that is in the Hunter population. Those patients will need enzyme replacement therapy. That gene therapy is injected directly in the brain, but you know, Hunter is a whole body disease, especially you know, issues with growth, height, liver, lung. We've you know, mentioned this before. And so most of those patients, and in fact, we have several patients that have had previous gene therapy that are on the phase I, II study. So we see that eventually all patients will need to go to ERT, and ideally, that would be Tivi that they go to. And it almost obviates even the purpose of having gene therapy if you're gonna- Yeah, I- end up on a blood-brain barrier Yeah, I- Crossing enzyme replacement therapy at the end of the day anyways. Right. Well, and I think that's one question we get a lot, and I think is... Because we talk about blood-brain barrier crossing, a lot of people think, "Well, this just treats the brain," but actually it's IV delivered, and it's systemic delivery, and the peripheral endpoints I think have become even more interesting to us, just seeing the evolution of the data. Maybe we can talk about the timelines for the COMPASS confirmatory trial and what it is you're looking to show in that study. Yeah. So we completed enrollment of Cohort A at the end of last year, and we made the decision to expand additional nine patients as we're in this AA window. By the end of this year, the Cohort A will be done. Cohort B is not time limited. That's a peripheral, that's the sort of attenuated patients. So expect basically two years, from the end of this year as the timeline for COMPASS to read out. And the way we think about COMPASS is actually a couple points. So one is launch in the U.S. and then territories outside the U.S. that will, we can use the same data or named patient sales or whatever, basically, imagine another third of the market will be accessible prior to COMPASS. The last third of the market, we believe, at base case, will require COMPASS data, and this is Europe, generally speaking. And so that's kind of the way we look at COMPASS. We also think it's really important to have this very robust data set as we start bringing additional enzymes forward and being able to use biomarkers and say: Hey, here's an example of how a biomarker translated to efficacy, and here's the whole data package, and now we can do this again and again with, you know, Sanfilippo, Hurler, Pompe, and, and I think that's why we've invested so much in this program. So you talk about the systemic benefits, the non-CNS benefits of the product as an enzyme replacement therapy. Why is that alone on its own not adequate to go seek European and global approvals? Yeah ... with the, you know, look, it may enhance the CNS activity, but at the very least, it says good, if not better- Yeah ... than what Elaprase can do. This is a conversation we had, I think, four years ago as we started to see this data, and we thought: Well, maybe a strategy is just get approval on peripheral. But fundamentally, we built the platform to solve the CNS, and we needed Hunter as the validation of that broader platform. Now, not that you wouldn't get that anyway, you know, post-marketing, and there is a... The reality is that if you're going to price at a premium, you need to show you have a premium product. And so I think it's also really important to show that your data is superior across biomarkers and clinical endpoints. But that is a fair discussion, and it comes up again and again. Now, interestingly, Sanfilippo doesn't have as much of a peripheral disease component, so there I think we made the right decision three or four years ago to focus on the CNS component of Hunter 'cause that can then be applied to what we're learning for Sanfilippo. Why don't we segue to Sanfilippo now? How big is that patient population relative to Hunter? And maybe kind of give us the next steps that you started to outline previously. Yeah. So with Hunter, the great thing is because you have an approved medicine, you know almost exactly what the epidemiology is like, and the vast majority of patients are on Elaprase. That's not the case for Sanfilippo, but we think roughly, you know, I think our estimates are about 1,500 worldwide, maybe 300-400 in the U.S., so it's similar, we think maybe slightly smaller than Hunter. Okay, got it. And then the next steps for that program? Yeah. So we, as I described at the beginning, we have agreed with the FDA on an accelerated approval path. It's 20 patients. We're finishing the enrollment of the last patients for that, you know, basically that, what will represent that data package, and we'll be kicking off the phase III. So we're basically finalizing what that phase III plan looks like. Interestingly, I think with today's guidance on rare disease evidence principles coming from CDER and CBER, that sort of fits squarely into what this confirmatory trial would look like, and likely it will be a single-arm natural history comparator if you look at categorically that disease. And that's actually what our discussions have been going towards in the last year with CDER, which surprised us because of our past experience in Hunter. Since there's not necessarily the Elaprase anchor on price for non-neuropathic, right? In the in- Right ... Hunter setting, would you envision a meaningful price premium for the MPS IIIA program over Tivi? Yeah, so I think it's definitely too early to discuss price, and there's a lot of dynamics around pricing right now that we're all very aware of. And obviously, when we think about the most favored nation, our pricing will be in the U.S. first, and hopefully that will be rest-of-world price ultimately. But probably a bit too early on Sanfilippo, but hopefully, we'll be discussing it soon, though. Yeah. So one of the aspects of Hunter that you highlighted for gene therapy is that, well, you're gonna wind up on the ERT anyways for the peripheral manifestations of the disease, but I guess in MPS IIIA, where there's also now some gene therapy competition, you don't necessarily have that same dynamic because you said it's much more CNS-oriented. Yeah. So what do you think about that, you know, the patient segmentation- Yeah ... who might be best suited for enzyme replacement versus gene therapy? Yeah, I'll add even one more complexity. The gene therapy that's being considered in Sanfilippo is actually a systemically delivered gene therapy, even though it's primarily a CNS disease. And part of it is, if you give a gene therapy early enough, I think you expect enough infectivity in the CNS. I think it's really gonna be a question of superior efficacy. And that's really the dynamic that we're banking on if, you know, as we look at our data mature, so. So, I mean, I think we're forming the tip of the spear, right? I'm not, and correct me if I'm wrong, but these may not be programs that get Denali as a whole to profitability, but form the foundation for additional enzyme replacement therapies. Is that kind of a fair premise to be working with? Yeah. So I think a lot of that depends on how much you spend, how big your portfolio is, and how it evolves over time. But I think you're exactly right. We see this as the foundation building, but we invented the transport vehicle not just to go after enzyme replacement therapies, although we think that's a fantastic place to build a franchise. We do believe that franchise has a lot of value over time. But as you can see, there's the U.S. launch, there's territories that will follow the U.S., and then there's, more broadly, Europe, so that's gonna build value over time. And maybe at some point, you know, yes, the ETVs will lead to profitability, maybe Hunter and Sanfilippo combined. But comes the next program, which is our Pompe program, right? And this, and that's why I spent a lot of time focused on this one. It may be very, very early, but on the other hand, now this is a patient demographic that, in combination with the other programs, can drive Denali in total to profitability as we kind of wait for the LRRK2 program and a little bit more visibility on Alzheimer's and beyond. So it just kind of helped frame the rationale for taking this approach in the Pompe and how you think you can differentiate. Yeah. So, I mean, the Pompe represents a couple of things for Denali. It's actually the first, I'd say, categorically, at least for LOPD, non-CNS indication, where it's a muscle delivery. It's a significantly larger population. The whole development plan will be different. This is not gonna be like Sanfilippo or Hunter, where there's, you know, we're not convinced that there's a biomarker that can lead to a very rapid accelerated approval. However, you can do, you know, active comparator or standard of care comparison trials relatively quickly, and I think that's gonna be the goal with looking at, like, six-minute walk test or other endpoints, including the biomarkers. But Pompe, for us, if you look at our data, what the ETV does is substantially improve the muscle endpoints. Obviously, it brings the CNS in, and so in IOPD, where there is clearly CNS involvement in infantile-onset Pompe disease, that we can clearly go after that unmet need with ETV GAA. But we actually are focused on the broader population here, and what we'd like to see is relatively quick biomarker proof of concept, and there's a set of standard biomarkers around glucose metabolism, around, you know, muscle damage that we can look at and have been looking at in our animal models, where we see clear differentiation versus the new standard of care or the new molecules that just recently launched. and I guess, where do you see the incremental unmet need for it relative to the new molecules? Are they not adequately depleting the glycogen storage, or glycogen buildup in the muscles? Right. It's probably, like, deep. I mean, if I'm thinking at a mechanistic level, it's probably deep targeting of muscle tissue itself, if you're asking the mechanistic. From a clinical perspective, it's still, you know, muscle weakness, respiratory over time, and that's gonna be the key to differentiate on those levels. I mean, do you have a target profile in terms of what... You know, if you really do optimally replace enzyme, can we start thinking about normalizing development of these kids? If not, why not? Yeah. So I think if you look at Pompe, a little bit like Hunter, and Sanfilippo, there's a lot of heterogeneity in the genetic risk and the heterogeneity of how the disease evolves. I mean, obviously, IOPD is, you know, categorically different than LOPD, but it's probably still a spectrum. But that's where we'd like to go, is normalization, and that's where we have gone in Hunter and ultimately in Sanfilippo. And the goal, if you get there early enough and you can normalize substrate, you should have, you know, basically normal development in case of those diseases. And in this, in the case of Pompe, it's really about muscle strength and respiratory function. Yeah. Do we have a sense of the newly approved therapies, the extent to which they... Like, the percent reduction of- Yeah - glycogen and how much residual load there is that could be addressed? Yeah, that's... Again, now, we don't have to go back four years- Yeah for that debate. That's, like, last week at Denali as we were discussing the biomarkers, and understand, we believe that there are definitely room for improvement, but a little bit more heterogeneity. I mean, it's not like heparan sulfate, where you know, Elaprase didn't do anything to heparan sulfate in the CSF. Yeah. But actually, if you look at heparan sulfate in the periphery, it's really interesting. We see, you know, from tenfold elevated down to twofold, but it's still twofold elevated, and we still see a very robust effect. So that's the goal, is that you get rid of the heterogeneity in your response, and you have a, you know, basically a more robust reduction in, let's say, urine Hex4 or creatine kinase or whatever it is we're measuring, right? So, you emphasize the infantile onset form. Do you plan on going more broadly to the other forms of Pompe? Yeah, so I think actually the goal is to go after LOPD, and infantile is a great place for us to show, you know, an effect in the CNS, but that alone is not why we're developing the molecule, so very much a focus on LOPD. To be clear, you're starting with infantile onset. Was that clear? Did I get that right? No. No, No, no, yeah. Oh, I got that wrong. Yeah, yeah. I got that wrong. I think the way to look at it is we're working on them in parallel, but we see that infantile, you know, it's a much smaller population, and we think that our medicine will definitely work there, but that's not where we're going necessarily. Upper case I looks like lower case L. Yeah. Hence the confusion on my part. Exactly, yeah. Um- I mean, this is the first time I've... This is the most depth we've talked about this program, so you wouldn't find it anywhere else, so yeah. Are you thinking about deploying the platform towards other muscle indications? And if so, how are you kind of prioritizing? Yeah, it's a great question. Okay. I mean, as the transferrin receptor platforms have evolved, there are obviously those companies that are approaching delivery of oligonucleotides to muscle. You know, obviously to brain is, you know, an area that we've focused quite a bit on is oligonucleotide, you know, delivery to the brain. They have always been on the list to go after muscle, but the reason we haven't gone there is we wanna make sure that when we go there, we understand what the competitive landscape looks like and what the unmet need still is. And it may be the type of oligonucleotide, it may be that the doses are really high that are needed for the current platforms, and we can come in with a lower dose, and we can optimize the affinity. We have a fair amount of data in our Science Translational Medicine paper on the OTV, the Oligo Transport Vehicle, including muscle data that's in the supplemental data. We've spent a lot of time on that, but we have not announced any muscle targeting program beyond Pompe. And I guess you alluded to knock down targeting muscle, but there's kind of similar to Pompe- Yeah ... other diseases where you could enzyme replace with improved therapeutic profiles. Right. MPS IV, if I'm not mistaken- That's right ... could be one. Yeah. Yeah. On the list, yeah. Okay. No, and I think actually what's interesting here is that a year and a half ago, as we were kind of at a point where the company had a choice, which is, you know, do we enter in a partnership? Do we raise additional capital? And really in an opportunistic way raise capital with really the mandate to do two things. One is to accelerate. Now, we didn't realize that that would mean accelerated approval. This was pre-Reagan-Udall Foundation meeting and sort of the evolution, which I think is fantastic, but the other was to expand. And so we are looking at where does the TV give us enhanced efficacy across therapeutic areas? So obviously, founded the company to cross the blood-brain barrier, but muscle is a great example. Bone is another great example where the TV... And so these programs are, you know, we don't talk a lot about them, but they will move. They can move very rapidly, and they may move rapidly in partnerships, or they may be our own programs, depending on the size of the indication, so. I mean, it's such an interesting conundrum, right? Which do you pursue on your own, because each one will have its own risk profile- Yeah ... and each one will have its own addressable market profile. And you must be asking yourself, like, how much risk are we willing to take on our own, you know, maybe to pursue some larger indications where the targets aren't quite as validating- Right ... as opposed to, you know, hey, we're gonna be the next Genzyme, right? The next BioMarin. We're gonna take all these enzyme replacements and just upgrade them- Yeah, yeah ... in a very modular, predictable, low-risk kind of way, but not necessarily with the same large patient populations- Yeah ... to address. I mean, I don't know how many companies you sit down with have a enzyme replacement therapy portfolio and an Alzheimer's portfolio, but that's sort of the spectrum of what we're working on. And in fact, we'll be bringing our first OTV into the clinic very soon against, you know, an Alzheimer's target. And then we just had a paper in Science three weeks ago on our ATV, A-beta, and reduced ARIA, improved plaque reduction. This is obviously a very hot field. That molecule goes into the clinic next year. We've selected the lead arms for A-beta. So you think about the risk spectrum, we could be an enzyme replacement therapy company only, but this technology allows you to go after a broader area, and it's how to be selective in that and how to have a balanced portfolio with risk and opportunity. Now, one thing that's interesting is there's a lot more interest, not surprisingly, in partnering in these large indications, especially now that the barrier has been broken for Alzheimer's, and you have a couple approvals, and you can get, you know, better medicines now. This is area where you see a lot of interest and a lot of partnering happening. I think, again, over the last 10 years, if it shows anything, we'll be opportunistic about how we advance our portfolio. So you have too much going on to cover in one session- Yeah ... but maybe in the final seconds here, just kind of lay out some of the other milestones we should be looking towards over the next, say, 12 - 18 months for the other programs in the pipeline, FTD, LRRK2, et cetera. Yeah. I mean, ideally, by this time next year, we have a launched product. We're preparing for another AA filing. We have, let's see, one, two, three, four additional TVs in the clinic. We didn't talk about progranulin, but that would be one of those, two in Alzheimer's, another ETV, and then our goal is one to two INDs per year, but that's basically where we'd be in a year from now, including, you know, hopefully a successful commercial launch in Hunter. So a lot going on for sure. Excellent. All right, Ryan, thanks so much for joining. Thanks, everyone, for coming out and tuning in. Thanks.