Great stuff, Ohm.

So is it reasonable to say that part of an MOA vs. NASH might be:

1) Leron downregulates sPLA2-11A;
2) sPLA2-11A induces production of arachidonic acid;
3) Arachidonic acid induces free radicals;
4) Free radicals are implicated in, among other things, hepatic Steatosis (overproduction of fat in liver);
5) hepatic steatosis leads directly to non-alcoholic fatty liver disease.

This is in addition to protecting mitochondria.

Is this how you see the chain of events?

Thanks.