It is difficult to determine whether mitochondrial dysfunction and oxidative stress are primary events or a consequence of inflammation in NASH development; however, as suggested by the increased gene expression of antioxidant catalase and GPx-1 and protein expression of GPx-1 and SOD-1, the beneficial effects of ASA and MitoQ seem to be correlated with a decrease in oxidative stress [7]. This evidence concerns the gene GPX1 and metabolic dysfunction-associated steatohepatitis.