Accordingly, mice deficient for PPARγ present alterations in renal lipid metabolism, and the extent of renal damage induced by a high-fat diet is lower in PPARγ heterozygous knockout mice than in wild-type mice concomitant with a decrease in lipid accumulation and lipogenesis and an attenuation of lipid-mediated kidney damage [33]. The gene discussed is PPARG; the disease is Nephropathy.