CYP2E1 and metabolic dysfunction-associated steatohepatitis: This CYP2E1 stabilization in CHIP−/−-mice was associated not only with a correspondingly increased functional activity, but also with increased lipid peroxidation with concomitantly increased 4-hydroxynonenal tissue conjugates and 15-F2T-isoprostane levels, marked activation of the hepatic JNK-cascade and microvesicular fat accumulation quite early at 2 months, which within 8–9 months of age progressed to macrovesicular fat accumulation, hepatocyte ballooning and injury, typical of clinical NASH [29].