The initial process of carcinogenesis, driven by genetic alterations, is followed by subsequent modifications (i.e., mutations in KRAS, TP53, CDKN2A, or SMAD4), depicted as dysplastic changes in flat lesions called pancreatic intraepithelial neoplasia (PanIN) or cystic lesions, such as the most prevailing intraductal papillary mucinous neoplasm (IPMN)5. This evidence concerns the gene KRAS and pancreatic intraductal papillary-mucinous neoplasm.