Notably, the administration of LXR ligands also activates lipogenesis by enhancing hepatic fatty acid synthesis through the upregulation of sterol regulatory element-binding protein 1c (SREBP-1c) and carbohydrate response element-binding protein (ChREBP), resulting in hypertriglyceridemia and hepatic steatosis [37–39]. The gene discussed is MLXIPL; the disease is fatty liver disease.