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This thread is aimed at the lay public - we already reported our findings, and shared all our data, with the genetics community on 27th September. So I've glossed over some nuances which we discuss in the paper.
The biggest limitation is that the genome is complicated and our predictions are based on the assumption that there is only one mechanism linking the genetic variant to the clinical consequences. That's why I keep saying no-one should treat patients on thia evidence. Need trials.
The key point is that this is big progress, but not an answer. If one third of our drug predictions from genetics lead to effective drugs, that's much better than the current success rate in trials in covid. And infinitely (literally) better than the success rate in sepsis.
One example of the kind of complexity we see is that there are other genes near TYK2 that may also affected by this variant - e.g. ICAM5. It's possible (but less likely based on the evidence) that this is the explanation for the effects we see
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