Multiple combinations of genetic mutations are commonly observed in PCs and can be classified as mutational activation of oncogenes, predominantly KRAS, found in >90% of pancreatic cancers; inactivation of tumor suppressor genes such as TP53, p16/CDKN2A and SMAD4; inactivation of genome maintenance genes, such as hMLH1 and MSH2 (most of these mutations are somatic aberrations), which control DNA damage repair; and alterations in genes specifically involved in the homologous recombination repair pathway, such as BRCA1 and BRCA2 (most of these mutations are germline) [24]. This evidence concerns the gene TP53 and familial pancreatic carcinoma.