Several secondary bile acids, including tauro-β-muricholic acid (T-β-MCA) [1], glycoursodeoxycholic acid (GUDCA) [2, 10], and hyocholic acid (HCA) [4], have been identified as endogenous FXR antagonists that improve metabolic endpoints in mice with established obesity by inhibiting intestinal FXR signaling. The gene discussed is NR1H4; the disease is Obesity.