Nevertheless, dacomitinib can downregulate the ABCB1 and ATP-binding cassette subfamily G member 2 to antagonize the efflux function of hepatocytes,[29,30] increasing the risk of intrahepatic cholestasis; while dacomitinib itself was mainly metabolized in the liver, 79% was excreted in the feces, of which 20% was excreted in the prototype form. This evidence concerns the gene ABCB1 and intrahepatic cholestasis.