“…Of note, these changes in FGF19 also correlated with increased serum C4 (a marker of hepatic BA synthesis), suggesting that low FGF19 might be a relevant driving force for the emergence of BA overproduction and BA malabsorption (BAM), a feature frequently found in CD [88,89]. From a more general point of view, it is also tempting to speculate that alterations of the enterohepatic FGF19 signaling axis could contribute to the pathophysiology of some other liverspecific complications (e.g., gallstone formation, primary sclerosing cholangitis or NAFLD) that are frequently associated with IBD [90][91][92]. Recent studies also started to elucidate the potential role of the BA-FXR-FGF19 axis for other enterohepatic co-morbidities (i.e., short bowel syndrome/intestinal-failure associated liver disease), suggesting that the impact of FGF19 on liver health might be very broad even beyond IBD [93,94].…”