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. This evidence concerns the gene NR1H4 and obesity due to melanocortin 4 receptor deficiency.