Consistent herewith, we further demonstrated that loss of Prdm3 not only increased the severity of cerulein-induced pancreatitis, but also accelerated cellular atypia and tumorigenic potential in the pancreas, as Prdm3-deficient mice undergo robust formation of precursor lesions in the presence of oncogenic Kras. These findings implicate a potentially protective mechanism of Prdm3 in pancreatic exocrine cells, which is different from the pro-tumor role of PRDM3 in several aggressive forms of cancer including colon, breast and ovarian cancer28–30. This evidence concerns the gene MECOM and neoplasm.