NR1H4 and intestinal cancer: Intriguingly, INT-767-enriched diet administered to mice carrying a germline mutation of the Apc gene, where inflammation is not the major drive of the spontaneous onset of intestinal cancer, corroborates the finding that, more than the mere direct attenuation of inflammatory pathways, INT-767-dependent Fxr activation, and the associated Fgf15 prompt, inhibits hepatic BA synthesis as demonstrated by Cyp7a1 decrease.