Consistently, the in vivo study also suggested that overexpression of wild-type BAP1 but not inactive mutant BAP1C91A evidently inhibited ICC progression, and the immunohistochemical results also confirmed that the inhibition of ERK1/2 and JNK/c-Jun signaling pathways were mediated by wild-type BAP1 but not by inactive mutant BAP1C91A (Fig. 4e, f). Here, JUN is linked to intrahepatic cholangiocarcinoma.