Oncogenic Ras requires activation for pathological levels of activity

High Ras activity generated by these stimuli led to acinar cell senescence and generated inflammation and fibrosis resembling the histological features of chronic pancreatitis (CP) with abundant mPanINs that spontaneously progressed to metastatic PDAC only in animals expressing physiologic levels of oncogenic Ras. Since a large population of normal healthy humans harbors Ras mutations, a reduction of factors that can activate Ras signaling may have important therapeutic and preventive value.