However, GNASR201H and GNASR201C greatly accelerated the onset of IPMN in the presence of mutant KRAS without frank tumor formation [139–141], and in response to the loss of p53, GNAS/KRAS-double mutant neoplasms swiftly progress to invasive PDAC [141]. Here, KRAS is linked to pancreatic intraductal papillary-mucinous neoplasm.