Dietary models gain weight, develop steatosis, and become insulin-resistant, but exhibit much less liver injury than human NASH patients, suggesting fundamental differences in rodent and human livers.[5], [48] Indeed, metabolic profiling of rats fed a methionine-choline-deficient diet—which inhibits fatty acid oxidation, thereby leading to NASH—identified species differences in bile acid, insulin, and leptin levels,6 limiting this model’s utility for studies of biomarkers or disease progression. This evidence concerns the gene INS and metabolic dysfunction-associated steatohepatitis.