However, a clinical sequence study has indicated that KRAS is mutated in more than 90% of cases of pancreatic cancer, with frequent associations with other mutations, such as mothers against decapentaplegic homolog 1 (SMAD1) family in the transforming growth factor beta 1 (TGF-β) pathway, and tumor suppressor genes, including tumor protein P53 (TP53) and cyclin-dependent kinase inhibitor 2A (p16Ink4a) [56]. This evidence concerns the gene CDKN2A and familial pancreatic carcinoma.