It is thus tempting to speculate that other ‘lean’ mouse models19, 22, 31, 32 that arise from defects in neutral lipid storage in WAT may also manifest a lipodystrophic phenotype with the development of hepatic steatosis and insulin resistance when exposed to a more extreme nutritional challenge as was previously reported for mice with a loss-of-function Pparg mutation33. The gene discussed is PPARG; the disease is Insulin resistance.