Our finding that ICC only developed in mice with homozygous deletion of Bap1 and Kras activation suggests that complete loss of Bap1 cooperates with oncogenic Kras to either preferentially drive the putative cell(s) of origin down the pathway of cholangiocyte differentiation and/or transdifferentiation of hepatocytes into biliary-like cells. This evidence concerns the gene BAP1 and intrahepatic cholangiocarcinoma.