It is reported that well-established lipodystrophy mouse models, such as Agpat2 disrupted mice and A-ZIP/F transgenic mice, develop severe lipodystrophy along with an elevation of a hepatic pool of triglycerides and upregulated hepatic de novo lipogenesis [34,35], suggesting that steatosis observed in lipodystrophy is complex, and hepatic de novo lipogenesis is, at least partially, one of the metabolic factors that contribute to steatosis. Here, AGPAT2 is linked to lipodystrophy.