Consistently, the treatment of soluble ACVR2B/Fc at 1.5 months old age, before PDAC develops, promoted the development of cystic lesions, which are reminiscent of a high incidence of IPMN by loss of activin A signaling during KrasG12D‐dependent tumorigenesis.[24, 29, 30, 31] Therefore, the consistent observations identify activin A as a risk factor predisposing to the development of IPMN when KrasG12D is present. Here, ACVR2B is linked to pancreatic intraductal papillary-mucinous neoplasm.