However, even with this apparently close association of CYP2E1 with both NAFLD and NASH and in several animal models of both alcoholic and nonalcoholic steatosis, Cyp2e1-null mice still develop diet-induced NASH or alcoholic liver inflammatory disease indicating that Cyp2e1 deletion neither prevented nor decreased oxidative damage [103–105]. This evidence concerns the gene CYP2E1 and metabolic dysfunction-associated steatotic liver disease.