Selective pharmacological activation of intestinal FXR has been shown to sufficiently elicit several beneficial metabolic and anti-cholestatic effects.[24], [25], [26] As such, intestinal agonism of FXR and the subsequent increase of gut-derived Fgf15, as well as administration of FGF19 and its mimetics,24,27 all known to suppress BA synthesis, reduced cholestasis in Mdr2-/- mice.24 Here, NR1H4 is linked to cholestasis.