The transgenic mouse models needed to have synergistic mutations of Gnas and Kras to develop a cystic tumor, while in human cases, IPMNs can develop with mutations in either GNAS or KRAS. In addition, the cystic tumor developed in the Tg-GnasR201H:KrasG12D mice always showed a gastric or pancreatobiliary phenotype. Here, GNAS is linked to cystic neoplasm.