Binding of FGF19 to the receptor leads to a negative feedback regulation on bile acid synthesis.32,33 In an FMT model for recurrent CDI patients, levels of FGF19 were significantly increased post-FMT, thus suggesting upregulation of the FXR-FGF pathway after FMT that may aid in C. difficile clearance.34 Furthermore administration of obeticholic acid, an FXR agonist, to HFD CDI-infected mice resulted in decreases in disease severity, and the use of ursodeoxycholate (UCA) in a CDI mouse model showed increased levels of FXR as well as TGR5 that modulates the immune response against C. difficile. The gene discussed is GPBAR1; the disease is clostridium difficile infection.