To investigate the molecular mechanisms by which Prdm16 controls PDAC progression and metastasis in the context of a Smad4 null background, we took advantage of our earlier IHC analysis showing that Smad4 deficiency in KSC mice was associated with a persistent de-repression of Prdm16 during the progression from IPMN to PDAC (Fig. 1 E). Here, PRDM16 is linked to pancreatic intraductal papillary-mucinous neoplasm.