KRAS and pancreatic neoplasm: Previously, with genetically engineered mouse models (GEMMs) and established cell lines of pancreatic tumor, we determined that Setd2 deficiency facilitated Kras‐induced pancreatic tumorigenesis.[8a] Strikingly, we observed a significant difference in proliferative capacity between Setd2‐proficient (Setd2WT) and Setd2‐deficient (Setd2KO) pancreatic tumors under in vivo condition that was not observed under in vitro culture conditions.