Combined with the current study, these findings indicate that pharmacologic antagonism of HNF4α suppresses NFκB binding to promoters in genes critical for canalicular bile export, and at least in part results in increased expression of BSEP, thus reducing exposure of the hepatocyte to toxic levels of bile acids and protecting the DSS-PN mice from cholestasis and hepatic injury. Here, ABCB11 is linked to cholestasis.