In the pathogenesis of NAFLD, the increasing accumulation of fatty acids in hepatocyte could ultimately result in reactive oxygen species being produced in mitochondria, peroxisomes and the cytochrome P450, CYP2E1 and CYP4A systems, causing lipid peroxidation and cytokine release leading to hepatocyte injury3, 20. Here, CYP2E1 is linked to metabolic dysfunction-associated steatotic liver disease.