This was evident in a mouse model of ANIT-induced cholestasis, where wild-type mice had a lower hepatic expression of the bile acid uptake transporter Ostβ and higher expression of the bile acid efflux transporter Bsep. Fxr−/− mice lacked this response, suggesting FXR-dependency, and were more susceptible to liver injury [92]. This evidence concerns the gene NR1H4 and cholestasis.