Notably, previous investigations both in mouse and human have demonstrated that Nupr1 cooperates with Kras not only during PanIN formation and PDAC development but, in addition, these two proteins arm frank pancreatic cancer with a more aggressive phenotype, characterized with poor survival and resistance to chemotherapy.24 Thus, the current study not only identifies for the first time senescence as a cellular mechanism linking the functions of these two proteins but also adds Nupr1 to the growing group of stress-associated proteins involved in the regulation of this process. The gene discussed is NUPR1; the disease is familial pancreatic carcinoma.