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Friday, September 11, 2015 2:23:13 PM
Rahul Jasuja - Noble Life Science Partners
And also the other question sort of stems from the fact that there is much said about connecting adapt -- innate immunity and there is a bunch of NK cell [ph] strategies in play as well. From the cytokine profile and looking at the translation work that you guys presented at ImVacS in the lung cancer. So you're seeing interferon [indiscernible] and other cytokines that -- and also converting M1 to -- M2 to M1 macrophages. How significant do you think your approach that [indiscernible] does that, but no other checkpoint inhibitor does that. Any color on that aspect when you could be connecting both the arms of the immune system have and deciding which tumors you're going to attack and how the combination approaches may pan out?
Steven W. King - President and CEO
Yeah I mean I think you've made a great point because what we're doing to this activating events in starting this immune response is basically taking away that natural defense the tumor has for stopping all immune responses, so that's both a native and adaptive killing of the tumor. And so we're really basically reversing that probably equally on both sides of the equation and we have good data that supports that.
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