But most appealing was the fact that Prdm16 expression in KSC mice did not follow this transient pattern of Prdm16 expression, increasing markedly in IPMN lesions but thereafter remaining constant in PDAC lesions (Fig. 1 E), suggesting that Smad4 might influence Prdm16 expression during the progression from IPMN to full-blown PDAC. Here, SMAD4 is linked to pancreatic intraductal papillary-mucinous neoplasm.