described that liver organoids with four common cholangiocarcinoma mutations (TP53, PTEN, SMAD4, and NF1) gained malignancy after loss-of-function of BAP1 by CRISPR/Cas9, because BAP1 could control the expression of junctional and cytoskeleton components by regulating chromatin accessibility (44). This evidence concerns the gene BAP1 and cholangiocarcinoma.