The carcinogenesis of pancreatic ductal adenocarcinoma (PDAC), comprising 90% of the pancreatic cancers, involves progressive accumulation of key driver mutations, usually leading to the activation of the KRAS oncogene and loss of the tumor suppressor gene TP53, contributing to the histological evolution of pancreatic intraepithelial neoplasia to PDAC [33,34,35]. The gene discussed is KRAS; the disease is familial pancreatic carcinoma.