​​Concerning carcinogenic risk, chronic FXR activation displays a complex tissue-selective duality:​​ while systemic FXR loss promotes hepatocarcinogenesis and tumor-specific FXR silencing characterizes the HCC/CCA microenvironment (131), hyperactivation within specific gastrointestinal tissues may drive β-catenin-dependent oncogenesis (132). The gene discussed is NR1H4; the disease is neoplasm.