KRAS, CDKN2A, TP53 and SMAD4 are some of the genes found to have been well described and commonly mutated in pancreatic cancer, with major downstream repercussions in their signalling pathways.3, 4 Given the regulatory functions of some of these common mutations in terms of maintaining controlled cellular proliferation, it is likely that important molecules involved in the replication machinery such as Cdc6 are implicated as well. This evidence concerns the gene KRAS and familial pancreatic carcinoma.