Similar mPanIN progression profile was observed in p16−/−; LSL- KrasG12D; Pdx1-Cre and p16flox/flox; LSL- KrasG12D; Pdx1-Cre mice as in LSL-KrasG12D; PDX1-Cre mice but at an accelerated pace (Fig. 4), indicating that biallelic inactivation of p16 accelerated the development of PDA in synergy with KrasG12D but did not alter the pathological progression of the pancreatic lesions- 20% of the pancreatic ducts in p16−/−; LSL- KrasG12D; Pdx1-Cre mice had mPanIN presentations around 4 weeks of age (Fig. 4), as opposed to >2 months in LSL-KrasG12D; PDX1-Cre mice [11]. The gene discussed is CDKN2A; the disease is Patent ductus arteriosus.