KRAS and adenocarcinoma: Mutation rate of K-Ras4B in PDAC can be as high as 95% [5,16,17] and accumulating evidence suggests that both calmodulin (CaM) and phosphatidylinositide-3 kinase (PI3Kα) play key roles in the K-Ras4B-driven adenocarcinoma [18,19,20,21].