NR1H4 and hepatocellular carcinoma: Recently, it has been proposed that the loss of FXR facilitates hepatitis B virus X protein (HBx)-induced liver cancer development in mice [73,74]; full-length HBx, but not C-terminally truncated variants of HBx, increased the FXR transactivation, thus the FXR-HBx interaction may exert a protective mechanism to inhibit HCC.