Although it is not known whether duct-specific expression of a GNAS mutant is sufficient to induce IPMN lesions, Pten loss or Lkb1 inactivation with KRas mutant expression in ductal epithelia drives IPMN-like lesions (Collet et al., 2020; Kopp et al., 2018), suggesting that IPMN-like lesions can be derived from ductal and acinar lesions in mice. Here, GNAS is linked to pancreatic intraductal papillary-mucinous neoplasm.