TP53 and metabolic dysfunction-associated steatohepatitis: ROS production and peroxidation resulting from FFA metabolism via oxidation trigger mitochondrial damage and apoptosis.5, 23, 24 p66shc has been suggested to mediate mitochondrial cell death pathways by increasing lipid peroxidation-induced apoptosis.25 Mice lacking p66shc were reported to exhibit increased resistance to ethanol-induced mitochondrial ROS generation and liver cell damage.27 Tomita K et al.26 demonstrated that p66shc was biologically active in the proapoptotic cascade triggered by p53 in an animal model of NASH.