Cholesterol has been shown to serve as an endogenous ligand for ESRRA [57,62,63,64,65]; thus, the significant increases found in cholesterol biosynthesis pathways and iWAT cholesterol levels in HF-fed LFABP−/− mice may be related to increased Esrra-mediated adipogenesis. The gene discussed is FABP1; the disease is hydrops fetalis.