Expression of a PDAC-associated mutant of Gnas, GnasR201C, and KrasG12D under control of the Ptf1a promoter is sufficient to induce dilation of pancreatic ducts and loss of acini, representing the IPMN phenotype (Ideno et al., 2018; Patra et al., 2018; Taki et al., 2016). Here, GNAS is linked to pancreatic intraductal papillary-mucinous neoplasm.