TP53 and Patent ductus arteriosus: While Kras and Trp53 transgene mutations are sufficient to induce PDA with high penetrance, a subset of the inactivating somatic mutations (2 of 10, 20%) and focal SCNAs (6 of 43, 14%) in KPC and KPTC mice were predicted to have a functional impact on mouse PDA biology by affecting genes previously implicated in key cellular processes25,34 (Supplementary Fig. 6, Supplementary Datas 8 and 9).