Thus, we provide evidence that long-term administration of INT-767 through FXR activation prevents spontaneous HCC development by controlling BA synthesis through Cyp7a1 reduction, limiting hepatic inflammation, proliferation, and fibrosis, consistent with the capacity of FXR to confer hepatoprotection and suppress HCC by controlling BA homeostasis12, 13, 38 and preventing hepatic inflammation and fibrosis37. This evidence concerns the gene NR1H4 and hepatocellular carcinoma.