This loss may cause the co-deletion of the tumor suppressor gene methylthioadenosine phosphorylase (MTAP), resulting in uncontrolled cell proliferation [131], as MTAP is located on the 9p21 chromosome, where CDKN2A/B is also located.CDKN2A/B and MTAP loss, p16INK4A methylation, senescence marker downregulation, and p53 alteration reflect fundamental genomic and epigenetic changes in Ov-CCA pathogenesis. The gene discussed is TP53; the disease is cholangiocarcinoma.