With regard to carcinogenesis of pancreatic ductal adenocarcinoma, well-known molecular alterations occur like telomere shortening, activating mutations in KRAS, inactivating mutations or epigenetic silencing of p16/CDKN2A and inactivating mutations in TP53 and SMAD4 leading to pancreatic intraepithelial neoplasia (PanIn) formation and, finally, to invasive ductal adenocarcinoma (45). This evidence concerns the gene CDKN2A and pancreatic ductal adenocarcinoma.