TP53 and cholangiocarcinoma: As shown in Figure 3, this schematic diagram summarizes that multifactorial mechanisms that are potentially involved in the ARID1A-driven CCA development, including opposing functions in cell cycle arrest, chromatin remodeling and chromosome organization, oxidative stress damage, DNA hypermethylation, downregulation of IDH, and the interaction of multiple genes (i.e., TP53, ALDH1A1, and Beclin-1 target) that enhance cellular proliferation and anti-apoptotic processes.