The extent to which the progression to NASH and fibrosis may have been ascribable to oxidant-dependent cell death and ensuing inflammation, or otherwise to the oxidative inactivation of tyrosine phosphatases and the promotion of STAT1 signaling in hepatocytes to drive T cell recruitment, inflammation, and cell death, as we noted previously (32), remains unclear. This evidence concerns the gene STAT1 and metabolic dysfunction-associated steatohepatitis.