Although hepatic PPARγ expression is relatively low under nonmetabolically stressed conditions (18), hepatic Pparγ expression is increased in obese and diabetic mouse models (19) as well as in human NAFLD (8, 20), and hepatic overexpression of Pparγ provokes fatty liver development in mice (21, –, 25), whereas liver-specific inactivation of Pparγ in ob/ob and AZIP mice reduces hepatosteatosis (26, –, 28). Here, PPARG is linked to metabolic dysfunction-associated steatotic liver disease.