Intriguingly, concomitant ablation of Prdm16 in KSC mice also resulted in a shift from IPMN to PanIN, which could conceivably contribute to metastasis in KSPrC mice, as the vast majority of PDAC GEMMs that develop PanINs also develop highly metastatic PDAC, including KSPC mice (Smad4 deletion and p53.R172H expression), which behave similarly to our KSPrC mice (Bardeesy et al., 2006a; Bardeesy et al., 2006b; Tuveson et al., 2004; Whittle et al., 2015). The gene discussed is TP53; the disease is pancreatic intraductal papillary-mucinous neoplasm.