To investigate the potential association between IRF8 and hepatic lipid metabolism, we utilized four murine models: leptin receptor-deficient mice (db/db), leptin-deficient mice (ob/ob), C57BL/6J mice fed an HFD, and C57BL/6J mice fed an HFD supplemented with high cholesterol and high fructose, all established models of NAFLD.16 This evidence concerns the gene LEPR and metabolic dysfunction-associated steatotic liver disease.