NR1H4 and cholestasis: In addition, the majority of the administered Gly-βMCA followed a gut microbiome deconjugation-dependent absorption route to enter the endogenous bile acid pool, and T-MCAs derived from Gly-βMCA not only decreased bile acid pool hydrophobicity but also acted as FXR antagonists to induce hepatic CYP7A1, which was an undesirable effect in cholestasis treatment (24).