Although KRAS is mutated in more than 93% of sequenced human PDAC and is described as the initiating genetic event for cancer formation, studies using genetically engineered mouse models reveal that physiologic expression of oncogenic Krasmut alone can promote PanIN, but it is rarely sufficient for tumor development in pancreatic exocrine cells [4, 17, 18, 24–27]. Here, KRAS is linked to neoplasm.