Yeah, that’s a great question. I mean, it’s something we started thinking of since we identified this target. So let’s say MED16 or any other target, really, once such a target is identified, you can start thinking first on how can we design a way to inhibit or modulate the pathway in human tumors, right? This can be either done genetically, pharmacologically, or with other approaches...
Yeah, that’s a great question. I mean, it’s something we started thinking of since we identified this target. So let’s say MED16 or any other target, really, once such a target is identified, you can start thinking first on how can we design a way to inhibit or modulate the pathway in human tumors, right? This can be either done genetically, pharmacologically, or with other approaches. Then we’re thinking of, okay, how can we combine this with existing successful immunotherapies? If knocking out a specific gene of interest makes the tumor cells more visible to the immune system, what happens if you pair that with anti-PD-1, anti-PD-L1, anti-CTLA-4, any of the new immunotherapies that are actually in the multiple pipelines that we have at our disposal? Would that amplify responses even further? So effectively, the path to translation becomes quite natural. We first identify this gene of interest with our screening technologies. We try to define and understand its mechanism of action. Then we build a therapeutic that mimics the knockout effect. And finally, we integrate it with established immunotherapies to drive stronger and more durable anti-tumor immunity.
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