Leonard Schleifer: Yes. I don’t think George’s point, can be overstated. Cancer cures in serious advanced tumors are still far and few between. And there is still tremendous need which makes this a very dynamic treatment marketplace because people want that extra benefit because it’s not like they are getting cures. We haven’t cured lung cancer or we haven’t cured most serious cancers. So, the ability to have foundational individual treatments and then get more by combining them really does position us to leapfrog to use George’s word in the treatment paradigm out in the world because patients and their doctors are very sensitive to improve outcomes because there is still tremendous, tremendous need.
Ryan Crowe: Next question, Shannon.
Operator: Our next question comes from the line of Mohit Bansal with Wells Fargo. Your line is open.
Mohit Bansal: Good. Thank you for taking my question. Maybe staying with COPD, so talking to some KOLs and reading some papers. It seems like IL-13 has some implication into fibrosis as well. Now, so the question is, do you think there could be a beneficial effect of IL-13 blockade and its impact on fibrosis on COPD-4 and above blocking inflammation? And if yes, do you think a 1-year trial would be enough to see that?
George Yancopoulos: I think you bring up really interesting points. We were actually involved in some of the experiments years ago that showed that IL-13 could actually cause fibrosis in animal models. And certainly, we do believe that long-term, like in many of the diseases that we have studied so far, that the benefit of Dupixent and blocking both IL-4 and IL-13 can continue to accrue for the patient in terms of preventing the chronic inflammation that results in so much of this remodeling that you talked about. We believe this may be true in asthma. And we are actually involved in programs and studies to show that some of the same things that you are talking about will also benefit in that and you will prevent long-term remodeling that decreases lung function over time in structural changes in the asthmatic patients and we believe that, that may also be true, of course, in COPD.
But first, we need, as you say, the shorter term studies to be positive, but we do believe that if they produce the type of data that we hope if Dupixent type data, we are hoping it could in COPD, that longer term studies, like you say, could end up showing even longer term benefits in terms of exactly the type of remodeling and fibrotic changes that result in permanent loss of function, lung function in these patients. So, we think that you are totally right, but it will probably, as you say, take longer term studies to actually pick that up.
Ryan Crowe: Thanks George. Next question Shannon.
Operator: Our next question comes from the line of Colin Bristow with UBS. Your line is now open.
Colin Bristow: Hi. Good morning and thanks for taking the questions. I wanted to sort of push a little more on the COPD readout. And just trying to understand what’s underpinning your confidence here. It certainly feels like you are more enthusiastic than what we are hearing out of Europe. Is this primarily based on the threshold set for BOREAS interim and these were sufficiently robust that you just €“ you feel good about the ultimate result, or is there something else you can point us to? Thanks.
