Because mutational inactivation of PRDM16 has been shown to be associated with leukemia (Zhou et al., 2016), we went on to explore whether Prdm16 could contribute to the pathogenesis and/or progression of PDAC, in which acquisition of oncogenic KRAS endows acinar cells with stemness traits that facilitate their differentiation toward a ductal-like lineage, thereby culminating in acinar-to-ductal metaplasia and attendant emergence of premalignant lesions (Bardeesy et al., 2006a; Gu et al., 2003; Park et al., 2008; Tuveson et al., 2004). Here, KRAS is linked to leukemia.