Thank you for joining us here today for our fireside chat. We have with us from Roivant, Matt Gline, the CEO of the company. So to begin, I thought for people that are not as familiar with your story, maybe just give a brief overview of the company and what's important to you. Yeah, thanks, and thanks for hosting this. Thanks, I know there was a schedule change. Thanks for accommodating that. It's great to be here again. Yeah, so Roivant is a biopharmaceutical company. We have about a $9 billion market cap. We have about $6 billion in cash. We are a developer mostly of late-stage therapeutics. That's where most of our interest lies. And what we're really, really good at is identifying promising drugs, bringing them in, and pushing them through late-stage clinical development. We're set up in sort of a funny way, where we have this portfolio of mostly wholly but some partially owned companies called Vants that do our actual sort of tip-of-the-spear development work. And what we do at Roivant is find the opportunities, bring them in, and build Vants around them. Our pipeline at this point is mostly concentrated in late-stage I&I, with a really terrific franchise of, we think, best-in-class FcRn antibodies, as well as a really promising JAK1/JAK2 inhibitor. Just last week, we announced a new program outside of I&I in PH-ILD, which is an sGC activator that we're really excited about. Okay, great. So why don't we start at the top here? Your first commercial product was VTAMA for psoriasis. How has that progressed relative to your expectations, and what's next for this product? Yeah, so look, our thesis going in on VTAMA is you've got this market of psoriasis and atopic dermatitis patients who are mostly treated with topical therapy, mostly topical corticosteroids, have been for a really long time. And those drugs have some real limitations. They've got efficacy issues. They've got safety issues that mean you can't use the best ones in certain situations. And so we and a couple of other companies have gotten out there and tried to build a class of novel topicals or a category of novel topicals that address the liability of steroids or more efficacious therapies. You know, I think the hope was that docs would embrace the steroid alternative, and I think we've made some real progress, right? VTAMA is annualizing $80+ million, doing pretty good scripts. We got lots and lots of docs writing it. Obviously, it's been a slower churn than we would've wanted initially in psoriasis, but that's fine. It takes a long time to change a doc behavior. We have a PDUFA date in atopic dermatitis later this year, and AD is a much larger market, about four times as many patients. Our data is a little more differentiated there, so I think there's a real chance of a big uptake there. In general, it's just exciting to be out there with a drug that we think is a good drug. Okay, great. I do wanna ask you about your AD launch. So how do you think that will progress relative to what you saw in psoriasis, and how do you think about the peak sales potential of that product? Yes, so the market dynamics are different. It's a much larger patient population. There's about three to four times as many scripts. It's a market that's a little bit less well developed on the systemic side. Obviously, you've got DUPIXENT doing well, but other than that, everything's a little bit earlier in life, and then our data as a topical is probably more differentiated in AD than in psoriasis. So I think there's a lot of reasons to be optimistic. I think it easily could be a multi-billion dollar product in these markets together, certainly in AD. AD also has the dynamic of being a pretty pediatric market. There's a lot of younger patients, and our expectation is that our drug should be eligible to be prescribed all the way down to the age of two. That's the population in which we ran our phase III study, so it should be an exciting thing from that perspective. I think there's good reasons to believe the launch will be steeper and more sort of aggressive than it has been in psoriasis, but obviously, we'll have to see that when we get out there, and we're pretty excited just to sort of see it out to those patients. Okay, and then for the pediatric population, what does your competition in that market look like right now? Yeah, I mean, it's, it's pretty thin on the ground, to be honest, especially in the really young children. Obviously, steroids are approved. If you have a young child with psoriasis or atopic dermatitis, the first line always winds up being something like cortisone cream, so that's still out there. Other than that, most of the other novel topicals are either only indicated for age four and up or age six and up or are not yet indicated in a pediatric population. So for example, OPZELURA, another JAK inhibitor, I think has done a two to 10 or two to 12 study, but I don't think is yet labeled in that population. I think XELJANZ is still working on the sort of pediatric format. So, I think there's just fewer competitors and none that we're aware of that are very likely, with the exception of potentially OPZELURA, to get the label all the way down to two. Okay, great. So you have a pretty comprehensive FcRn franchise, and curious how you compare and contrast that with other FcRns that are in development and then some that are actually already approved? Yep. You know, what, what really sets you apart? Perfect. So look, in late-stage FcRn land right now, there are three to three and a half programs, really. There's nipocalimab at J&J. There's the sort of class leader, efgartigimod, VYVGART Hytrulo at argenx, and then there's us. UCB has a program that's more limited in scope, and then there's a couple of earlier FcRns that are sort of in early preclinical development or late preclinical development, but still remain to present themselves. Relative to the late-stage field, we think we've got some real advantages. So, especially our lead program, which is confusingly the one that's slightly earlier in development, IMVT-1402. So our whole franchise, we suppress IgG very deeply. That's first and foremost. Our drugs have been shown, both of them, to suppress IgG. We expect up to 80%+, maybe as high as 85%, which is deeper than, for example, efgartigimod has been able to show. And deeper than J&J appears to be taking nipocalimab in clinical studies, because of, we think, an albumin and potential LDL issue that they have, that our first-gen, batoclimab, also has. So the first thing is we suppress IgG more deeply, and that should just lead to better efficacy. Like, we believe across indications, deeper IgG suppression is gonna yield better clinical benefit to patients, so it starts there. On top of that, and this field is changing, but, our drugs, both of them, are straightforward subcutaneous injectables. IMVT-1402, for example, we think will be a simple auto-injector at launch. That compares with nipocalimab, which is still today being studied principally in an IV format, although there is talk of a SubQ Infusion device of some kind, and VYVGART, where VYVGART itself is an IV-only product, but VYVGART Hytrulo is their SubQ, is a Halozyme SubQ that's about a five cc, 30-second push with a high rate of injection site reaction, so we think in addition to better clinical benefit, we should have a cleaner route of administration that should get us access to a bigger patient population that way also. Okay, got it. And then for batoclimab, I see that you're actually still developing that into multiple trials, and what's your thinking behind that, and which indications do you think are most important for batoclimab? Yeah. So the beautiful thing about FcRn as a target is IgG suppression has been a great biomarker, and so across studies, if two drugs suppress IgG by the same amount, their clinical efficacy has been pretty similar. And so our view is, is that's true, and that means that all of the development that we're doing in batoclimab, among other things, can perfectly inform development work, progress, commercial prep, et cetera, for IMVT-1402, because we expect we'll suppress IgG the same amount. So, we were running a phase III program for batoclimab before IMVT-1402 itself. And so, you know, our original intention was to progress batoclimab in multiple indications. Once it was clear that IMVT-1402 had the potential that it did, we've mostly backed away from plans to launch any new studies in batoclimab, and so we have the ability... These are, in many cases, registrational studies. We have the ability to launch it in the event that the data is spectacular, but we also have the ability to use it to inform a IMVT-1402 development program. You know, in terms of where I think that data is gonna matter a lot, the thing that's most important from all of our batoclimab studies, which is the same as one of the things that was important from our Graves' data, that we read out just last week, is helping to underscore the extent to which deeper IgG suppression will matter from a clinical perspective. And so we've now shown that, I think, pretty conclusively in Graves' disease, but I suspect people will watch very closely what we show in myasthenia gravis, for example, 'cause it's such a large market already for VYVGART. I think it requires relatively little imagination, and so my hope is that we're able to show in that batoclimab study that the deeper IgG suppression of the 680 mg dose performs better than the 340 mg dose, and therefore, that sort of fast-forwarding that we ought to be able to have a best-in-class product from an efficacy perspective, overall. What kind of data do you have that really shows that higher IgG suppression actually leads to better efficacy? Because some in the field don't necessarily agree with that. Yes. So look, this has been shown in a lot of different settings at this point. Argenx and J&J both over time have shown in their data presentations that at the individual patient level, for example, in myasthenia gravis, MG-ADL, improvement is better in patients with... in individual patients with deeper IgG suppression. UCB showed in an ITP study where they did good dose ranging, that deeper IgG suppression mattered there. The J&J Sjögren's data that was presented back in June showed a pretty clear dose response, where as they escalated IgG suppression, they continued to deliver better clinical benefit. Obviously, we showed something similar in our TED data a couple of years ago, that in TED, at a deeper IgG suppression, we delivered more competitive efficacy benefit in TED. And then probably most importantly, the Graves' data that we put out last week. That study was not designed specifically to show a comparison between high and low dose, or deep and less deep IgG suppression. But as it worked in practice, the patients were treated for 12 weeks using our 680 mg dose, which suppressed IgG in this study by 77% on average, and then by 12 weeks at our 340 mg dose, that suppressed IgG by 65% on average. And we saw a pretty significant reduction in benefit, especially. So the way the study worked, patients were allowed on background antithyroid drugs, and so most patients were able to be euthyroid on either dose. It was about, what, I forget the exact numbers, but like 70% something in the 680 arm, and then 60% something, maybe 68% of the 340 arm. But the 340 arm required significantly higher ATD doses. And so if you looked at the rate of patients who were able to completely get off ATDs, it was like 56% at 680, and fell down into the 30s once you dropped to 340. And that's despite the fact that these patients in the 340 arm were getting a residual pharmacokinetic benefit, not really arm. In the 340 portion of the study, we're getting a residual pharmacokinetic benefit from the period during which they had been on high-dose FcRn. So we thought that was pretty compelling data for showing that dose matters. Okay, and do you have any bridging studies to show how batoclimab dose translates into IMVT-1402? Because I think one of the questions that we get from investors is: Don't you waste some time or lose some time by switching from batoclimab to IMVT-1402? Yes, so we did our preclinical work in NHPs, effectively a head-to-head comparison between high-dose BATO and IMVT-1402, and we've pretty well established for ourselves that IMVT-1402 does what it needs to do. The phase I study was very clear, we suppress IgG as deeply as we need to. It really does sort of work, and not only that, but it does not. The whole reason we developed IMVT-1402 was because batoclimab has an impact on albumin levels, and therefore an impact on LDL cholesterol, and IMVT-1402 does not have either. So that was an important thing for us to be able to show. Do we lose some time? Look, the mechanical answer to that question is, as an indication like MG, definitely, in the sense that batoclimab is reading out a phase III program early next year, and batoclimab would be approvable on the basis of that study, we think, and so we could launch BATO, but it will, it will come with that [attendant] LDL issue. Now, the thing that I said earlier about IgG suppression being a very good proxy for clinical benefit, though, what that means in practice is, we are no further behind than any other drug that is in or has recently read out phase II data, because anyone's phase II study is everyone's phase II study. Once you have established what 65% IgG suppression means from a clinical benefit perspective, you can go straight to FDA with IMVT-1402 and begin a pivotal program, and we're about to show that, for example, in Graves' disease, where our phase II data was generated with batoclimab, and we're now gonna launch a pivotal registrational program in IMVT-1402 imminently on the basis of that data. Okay, great. So you recently released what I thought was stellar data for Graves' disease. Thank you. The stock didn't really move. Based on your discussions with investors, what do you think people really miss? If I were better at predicting investor reaction to data and how the stock market moved, I could sit on that side of this table instead of on this side of this table. What do I think investors missed? Look, first of all, and I think this is probably the long-term biggest thing. Graves' is a disease that requires some imagination right now, right? There has not been a novel therapy in Graves' disease basically ever in modern biotech history. Mm. These docs haven't studied novel therapies. Investors haven't invested in novel therapies in Graves' disease. So it's just not the kind of place where if you're, say, a lazy pattern matcher, you can just wake up and know what you're gonna see. Not to call investors lazy pattern matchers, but just for example. And so, you know, look, I think what it's gonna take ultimately is people need to do the work. They need to talk to the docs, and the docs themselves, by the way. It's not like there's a well-established core of Guidepoint KOLs in Graves' disease. They're not used to getting these phone calls. Mm. So we need to work with the doc community to get people to think about the world in a different way. Investors need to do the work to talk to those docs. They need to sort of understand the patient dynamics, the payer dynamics. I think it's just gonna take a little bit of time, and I don't think that means they're missing anything necessarily. I just think people need to do their work. Whereas in a disease like myasthenia gravis or PH-ILD, which maybe we'll talk about later today or whatever, investors already just, like, have a clear, intuitive sense for those markets. Graves' doesn't have that. I'll say, though, I've probably done somewhere between two and three dozen, probably three dozen investor calls since Immunovant put that data out at the beginning of next week. Not one person has raised a substantive concern for the quality of the data. That is, I think the data has spoken for itself in terms of its quality, and where I think people feel the need to do work now is just understanding what Graves' could be and how to think about it, especially in a world where there's really no other competitor or comparator to point to. So that's most of what I think is gonna take a little bit of time. Now, the one thing that is encouraging to me is investors who have done work on Graves', I think have come away pretty impressed. And so my hope and expectation is the more people do that, the more we'll start getting credit for the data. Got it. So one of the things I thought... still thought was interesting is the potential for you to get a remission claim in Graves' disease. Yeah. What do you think about that opportunity, and how long do you think it will take for you to get something like that into your label? Well, so the primary endpoint of the study that we're gonna run in Graves' is patients being euthyroid, that is, having normal thyroid hormone levels and off ATDs. Those are the things that patients want most of all. Remember, the patient population that we're treating, this is a last-line therapy. These patients are fully refractory. Their only other option is a surgical excision of their thyroid or radiation of their thyroid. They are uncontrollable on any thyroid drugs like methimazole. What they want is to be controlled. Having out-of-control thyroid hormone levels sucks. Mm. You feel tired. You can't control your weight. It's like a miserable place to be. It has elevated rates of cardiometabolic disease and things like that. Like, it causes real problems. You can develop TED, which is a different and problematic condition, and so, you know, I think the first thing is patients wanna get controlled, and they wanna get off ATDs, which are, A, annoying to take, and B, have some side effects. So that's the primary endpoint of the study. The study is also designed to show the possibility of drug-free remission, and so there is an arm of patients who are on drug for a period of time and then taken off drug for a period of time. The good news for that is, look, our expectation is that placebo patients are not gonna spontaneously remit. It's very uncommon. Occasionally, you see patients who are controlled on methimazole wind up being able to get off methimazole, but it's very uncommon for patients to spontaneously remit. So there won't be a lot of placebo response there. Bluntly, no one's ever run a study like this with an FcRn before. No one's ever done this level of, like, autoantibody suppression, and so we don't know exactly what we're gonna see. But the study is designed to say, if we get patients controlled and off ATDs in 26 weeks, what is the probability that they can then go off an FcRn and still potentially show some remission? And I think we've got a reasonable chance of seeing that, based on the... Patients who are on methimazole and do get controlled by methimazole can sometimes go off methimazole after a period of stable therapy. So the hope is that we see a similar effect for uncontrolled patients who get controlled on FcRn therapy. Okay, great. One of the questions that we got from investors was why somebody would use your product, for example, in myasthenia gravis or some of the approved indications or will be approved ahead of you, when they're already stabilized on another FcRn. What, what do you... You know, how do you penetrate that market with established players in the market? I mean, look, our positioning specifically in myasthenia gravis will depend on our data in myasthenia gravis, right? If our data is not significantly better than, say, efgartigimod data in myasthenia gravis, I still think some patients may switch. For example, patients might not like the IV format of VYVGART. They may want to move to something they can use at home. They might not like Hytrulo, which is a SubQ that currently requires healthcare provider administration. But many patients, these were pretty sick patients before they went on VYVGART. If they're happy on VYVGART, I don't know that they're going to change. Now, the catch is, if our data, for example, shows IMVT-1402, that the batoclimab at a high dose, or ultimately implies that IMVT-1402 at a high dose, will deliver a better benefit on MG-ADL, that patients will feel better on our drug than they do on VYVGART, then I think we'll take a lot of share, because ultimately, what these patients want is to feel better. But I think that's going to have to be driven by the quality of the data. If our data is comparable, we stil l think SubQ is going to matter a lot. But in a world where our data is comparable in MG, I think we'll take less share in MG than in all of the other markets, like, say, Graves' or maybe Sjögren's, or any other disease where we will launch much closer in time proximity to VYVGART than we will in MG, where they're going to have a multi-year lead. And so there won't be patients who are ultimately on stable therapy on these other FcRns by that point. Okay, great. So you did mention that you also announced some positive phase I-B data on mosliciguat, and I'm curious the opportunity in PH-ILD, and then how you compare and contrast with other companies that are developing similar products to address that market opportunity. Yeah, perfect. So what's great about PH-ILD as a market, having just finished the conversation about Graves' disease, is if you are a lazy pattern matcher, you know a lot about pulmonary hypertension. There have been pulmonary hypertension drugs in development in biotech for a very long time, and PAH, this Group 1 pulmonary hypertension, is a huge commercial market with, I think, 15 approved agents. Obviously, Actelion was acquired for $30 billion on the basis of pulmonary hypertension. You've got United Therapeutics. It's a big company doing really great, actually, in PH-ILD. I'll come back to that. This is a market that investors are very familiar with, and even Group 3, even PH-ILD, we now have a roadmap, right? TYVASO, the United Therapeutics product, is approved in PH-ILD. It's probably doing $800 million annualized and growing at a good clip. PH-ILD is a... It's a horrible disease. It's a great pharmaceutical opportunity in that we know how to treat pulmonary hypertension. We've known it for a while. This is a sick subset of pulmonary hypertension patients for whom there are actually very few options. Unlike PAH, where there's, again, 15 approved therapies, really the only novel approved therapy in pulmonary Group 3, in PH-ILD, is TYVASO. TYVASO is a prostacyclin. It's a tough drug for pulmonary hypertension patients with... So PH-ILD is the subset of pulmonary hypertension patients with interstitial lung disease. These are people with sick lungs, and prostacyclins are hard for that patient population because, for example, an on-target effect of TYVASO is cough. Mm. And so you're taking these patients with sick lungs, and you're giving them a drug that causes them to cough more. It's pretty difficult. And on top of that, TYVASO, in addition to an on-target effect of cough, is a four-times-a-day drug with, in some cases, up to 48 puffs over the course of a day of the drug. That's also potentially inflammatory of the lung and sort of the whole breathing apparatus. So anyway, there's clearly an opportunity to add additional options for these patients. There are a number of people studying alternative formulations of TYVASO, basically. Mm. But other than that, there is not a lot novel in the late-stage development pipeline, specifically for PH-ILD, and it is a market that is roughly equivalent in size, frankly, to the PAH market. And so, look, we're really optimistic about our ability to deliver something to these patients. Now, the other thing I'll say is, across pulmonary hypertension, PVR has been a pretty good proxy for clinical efficacy, and certainly, there are very few drugs that have shown a good PVR benefit that have not resulted in effective therapies. And we've shown, I think, the best PVR data that anybody has ever shown in a decent study. And so I think we're very excited about what that means for our likelihood of succeeding in PH-ILD. Okay, another product I wanted to switch gears to was your Priovant and brepocitinib. Yep. What's the latest you've said on the clinical development program? Yes, so, brepocitinib is a TYK2/JAK1 inhibitor. It's currently being studied actively in two indications now: dermatomyositis, where there's a pivotal study, registrational program, reading out in the second half of next year, and then non-infectious uveitis, which is an inflammation of the eye, where we put out some really, really promising phase II data, 24 weeks in, March, I think, or April, March, something like that. And so the 52-week data in that indication is coming soon. Meanwhile, we have effectively begun a phase III program in NIU, and so... Anyway, we will be announcing shortly, I'm confident, that the first patients have been dosed in that clinical program. And look, that's a really exciting opportunity. NIU, again, is a disease where there's very, very little late-stage development work happening, and of the approved, there's really only one approved, sort of quote, unquote, "novel" therapeutic for NIU, that's HUMIRA, and HUMIRA doesn't work very well. So I think brepocitinib should be a really good opportunity to deliver a benefit to a patient population that needs it. Okay, and when will we see data for DM and NIU? The dermatomyositis field program reads out the second half of next year. Okay. And that's registrational data, so if that study is successful, we will file on the basis of it. NIU, we're just starting the phase III program now, so it'll be a couple of years before we get data from the phase III program. We will get 52-week data from the phase II study pretty soon, this fall sometime, about six months after April. And so that'll be interesting to take a look at, but obviously, that's not necessary to inform the phase III program, given the quality of the earlier phase II data. Okay, so the big question everybody wants to know is, you've got all this cash, $6 billion, roughly. What are you going to do with it? Swimming pools. Plastics? Plastics. Look, first of all, I don't think that should be the big question. I think the big question should be: How is this existing portfolio of therapies going to evolve into an important combination of treatments for patients. That said, we have made no secret. First of all, that portfolio of therapies, especially the FcRn franchise, obviously is a capital-hungry franchise. We expect to develop it quite broadly. So some portion of our $6 billion balance sheet will be spent, about a third, I'd say, will be spent on the existing pipeline. Another approximately a third will be spent on new business development, so things like the clinical development for mosliciguat that we talked about, but we have our eyes set on a number of other programs that we like. This environment is the best environment in Roivant's history for finding programs to work on, especially from Big Pharma, where there are these sea changes in the strategy of most big pharma companies, and we see opportunities of a kind and quality that the Street will not believe until they see. Mm. And we're actively working on in-licensing those things. Those deals take a long time, but we're very excited about what we have our hands on. And then, we have capital beyond what we can reasonably spend on even those things, and so we're in the process of returning about $2 billion to shareholders. We bought back about $650 million of stock from Sumitomo in the spring, and we have an active share buyback program, as well. Okay. What's the latest on your COVID-19 IP litigation? It's hard to comment publicly on active litigation, but the case with Moderna has progressed nicely. We had the Markman hearing earlier this year. The next major step in that case is what's called the summary judgment phase of the trial, which will take place in the spring, which is where some important legal questions, like the applicability of this Section 1498 government contractor defense, will be decided, and then the actual trial will be a year from now. It'll be in September of next year, is when it's currently scheduled, and it's a jury trial, so we will get an answer on infringement pretty quickly thereafter. The case against Pfizer is also progressing. The date for the Markman hearing is set in December, and so all of that's moving forward. Okay, great. Anything I didn't ask you about or that we didn't discuss that you think is really important for the story? Really important, no. The only relatively near-term thing you didn't ask about is we have a readout in our anti-GM-CSF antibody, namilumab, in sarcoidosis coming before the end of this year. That is, Look, GM-CSF has been a tough target historically. It's shown some okay data in RA, but it sort of struggled to find footing. Sarcoidosis has been a tough indication historically, where people have tried and failed repeatedly. The biological fit between GM-CSF and sarcoidosis is good. GM-CSF is involved in the formation of macrophages, which lead to these granulomas that are the disease pathophysiology of sarcoid. So it ought to work from that perspective, but tough patient population, tough indication, so probably a relatively lower probability of success. Sarcoidosis affects, call it, 200,000 people, most of which have pulmonary sarcoidosis. If we are successful, it's a really big opportunity, so I think that one probably should be on people's radar as a potential source of upside, but not, in my estimation, something that people are valuing today. Okay. We only have a few minutes left, so I wanted to open this up to Q&A from the audience. Does anybody have anything they wanna ask? Okay, well, then, I will close by asking you, what is your vision for the company over the next five years, 10 years? Where do you want this to go? You know, I struggled to answer that question because on the one hand, I think the answer is sort of self-evident, right? We are a therapeutics company. What we are here to do is to deliver medicines to patients. That's what roughly every room in this conference has a CEO who is sitting in a chair like this one, saying the same thing. I think we're well set up to do it, and in particular, the reason I think we're well set up to do it is, and I've said this in other formats, but I think one of the things that's, like, interesting about our industry is, we've benefited a lot from the dogma of other companies, right? Like, people wake up in the morning, and they're like: "I'm gonna build a company that's gonna change the world using CRISPR," or, "I'm gonna build a company that's gonna change the world using mRNA," or, "I was a PhD student, and I studied this one cancer target, and I'm gonna dedicate my entire career to trying to prove that that target works. Mm. Roivant's dogma basically is that we don't have a dogma. Mm. Our whole thing is that, like other people in relentless and aggressive pursuit of that one scientific idea sometimes do amazing things, but often leave a whole bunch on the cutting room floor that is nonetheless incredibly important from a scientific perspective and can benefit patients, and we are here to sort of go anywhere. We're here to kind of follow the breeze in an industry where so many other people have this, like, very specific through lane, and so it's hard to say, right? Are we gonna be an I&I company? I mean, I can't say that, right? Like, our business exists in the space between other people's cookie cutters, and so it's not the pumpkin, it's not the skeleton, it's not the scarecrow. It's, like, the weird outline that forms when you take those three things off the sheet. And so, you know, what is the vision for that? It's to look like that weird little tree shape, but to make a really nice cookie out of it, and so, you know, I think that, that's where we're headed. But ultimately, again, the goal is the same. We think that approach is gonna result in a whole lot of treatments that matter for a whole lot of patients, and we expect we're gonna develop them successfully, we're gonna commercialize them, market them successfully, and we're gonna build a really big company on the back of that idea. Okay, great analogy, and with that, we'll end things here. Thank you very much.