So ARO-APOC3, as you saw the data that we knew about the severe hypertriglyceridemia populations is confirmed, and it’s very remarkable and is consistent. And as I always said, with these therapeutics, we have 100% response with regard to hypertriglyceridemia. So our initial plan to go with the two severe hypertriglyceridemia syndrome, the FCS or the SHTG, continue to be the same. What we are learning and I think that was a key feature of our Analyst and Investor Day is what is the unmet medical need in cardiovascular risk reduction in the next five to 10 years? And we believe that the LDL cholesterol issue is probably well taken care of and the rest of the risks come from different sources of lipid and lipoprotein, most of which are addressed with the ARO-APOC3 molecule.
So in conclusion, we see the opportunity where the unmet medical need is and ARO-APOC3 fit very well with those criteria. So it’s not about prioritization, but it’s really going to where the drugs have the biggest promise.
Christopher Anzalone: Yes. Look, I think that our development programs worked exactly as we design them to work. We have these two drug candidates that were clearly active and clearly had some overlap in their activity. And people would ask how we’re going to apply these two drugs to various patient populations. And our answer always was we need to look at the data, and that will guide us. That was not a satisfactory answer to some people, but that was the answer. And now do we have an interim look got a better idea about how these will help various patient populations. And so now I think we’ve got a good idea. Again, as Javier said, we don’t view this as prioritizing. We view this as just following where these drugs are going to have their greatest benefit in which patients.
Operator: And our next question comes from Ellie Merle from UBS.
Ellie Merle: For the initial pulmonary readout in the first half of next year, I guess what are you looking to see in terms of the degree of protein knockdown based on the dose levels that you’re studying in healthy volunteers? And I guess when you think about pulmonary delivery, I guess, what is proof of concept for the pulmonary platform look like from this readout or if perhaps we do wait for longer-term data?
Christopher Anzalone: Sure. Look, I think these are well-validated targets, particularly MUC5AC. But I think even RAGE and certainly MMP7. And so our thinking is that if we can see a well-tolerated, deep knockdown in healthy volunteers, that is a substantial clinical proof of concept. We will also have some data later in the year on — in various patient populations. But I think if we can see good consistent knockdown in healthy volunteers that’s well tolerated, I think that is giant leap forward for the entire platform and certainly for the individual candidates. With respect to how much knockdown we need, I don’t think we’re setting expectations for ourselves here. I think we want to see what we see. But our hope is that we see consistent and at least relatively deep knockdown. And if we can, I think that given the importance of these targets, I think that they will have disease-modifying effects.
Operator: And our next question comes from Joel Beatty from Baird.
Joel Beatty : For the lung programs, MUC5AC and RAGE, I think in your prepared remarks, you mentioned that both of these programs are going to reaching the top of the SAD cohorts and also flowing MAD cohorts. How do you decide the peak dosing of those? Is this kind of preset? Or are you looking at safety or efficacy markers?
James Hamilton: So the dose levels for the SAD and MAD are largely preset. And then as we go from one dose level to the next, we have an independent Data Safety Committee that reviews aggregate safety data and boats to allow dose escalation from the dose just completed to the next higher dose. Hopefully, that addresses your question.
