Additionally, the elevated level of some secondary BAs (free and conjugated UDCA, 7-KDCA, etc.)in gut promoted the synthesis and excretion of BAs with irritable bowel syndrome patientsby inhibiting intestinal FXR/ FGF19 signaling pathway [44, 53], which was beneficial to maintain in vivo glucose homeostasis [54]. The gene discussed is FGF19; the disease is irritable bowel syndrome.