Perhaps the most intriguing finding in this study was the persistent increase in Prdm16 expression during the progression from IPMN to PDAC in KSC mice, which at first glance seems to support a hypothesis in which Smad4 might function as a repressor of Prdm16 during PDAC progression, and hence conceivably that canonical TGF-β/Smad signaling might also repress Prdm16 expression. Here, TGFB1 is linked to pancreatic intraductal papillary-mucinous neoplasm.