Diabetic mice with hepatocyte-specific deletion of PPARγ had improved hepatic steatosis yet more severe IR, probably due to reduced insulin sensitivity in muscle and adipose tissues.129 PPARγ agonists reduced hepatic steatosis in patients with NAFLD possibly due to effects in adipose tissue, where PPARγ activation promoted adipogenesis in adipose tissue to decrease the fatty acids entering the liver.130 In addition, deletion of PPARγ in non-parenchymal liver cells including KCs and HSCs exacerbated liver damage and fibrogenic response to carbon tetrachloride (CCl4) challenge.131. The gene discussed is TBCE; the disease is fatty liver disease.