Duodenal adenocarcinoma, by contrast, exhibits a distinct mutational profile, including alterations in Kirsten rat sarcoma viral oncogene homolog (KRAS) (30-50%), TP53 (40-60%), adenomatous polyposis coli (APC) (20-30%), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) (10-20%), and inactivation of SMAD family member 4 (SMAD4) (15-30%) [19]. This evidence concerns the gene APC and duodenal adenocarcinoma.