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. This evidence concerns the gene TGFBR2 and Patent ductus arteriosus.