The observation that loss of Bsep and subsequent hydroxylation of the BA pool attenuates cholestatic liver and bile duct injury with inflammation and biliary fibrosis in the Mdr2−/− mouse model of sclerosing cholangitis might be attributed to reduced hepatic expression of the pro‐inflammatory key regulator Egr1 (and subsequent downstream targets such as Cxcl1 and Cxcl2) in Mdr2/Bsep DKO mice as well as in Mdr2−/− mice fed with THBA. The gene discussed is CXCL1; the disease is sclerosing cholangitis.