Although deletion of MED1 results in embryonic lethality at E11.5, the MED1 conditional knockout or mutant mice play an important role in adipogenesis through PPARγ, fatty acid oxidation through PPARα, mammary gland development through ER, liver steatosis through GR and constitutive androstane receptor (CAR), thermogenesis regulation through uncoupling protein 1 (UCP1) up-regulation, skeletal muscle function, and insulin signaling (Ge et al. 2002; Jia et al. 2004, 2009; Jiang et al. 2010; Iida et al. 2015). The gene discussed is UCP1; the disease is fatty liver disease.