Most GEMMs are established by combining pancreas-specific endogenous expression of a mutant Kras oncogene, which is mutated in 95% of human PDA cases, in combination with pancreas-specific endogenous inactivation of one or two tumor suppressors genes (Cdkn2a, Trp53, Smad4, Tgfbr1, and Tgfbr2) frequently altered in human PDA. The gene discussed is CDKN2A; the disease is Patent ductus arteriosus.