The canonical KPC (LSL-KrasG12D/+; LSL-Trp53R172H/+; Pdx1-Cre)15 mouse model—which combines an activating mutation in Kras, and a dominant negative mutation in Trp53—is one of the most-studied GEMMs of PDA and has been shown to closely recapitulate the biology of human PDA in terms of histopathological and clinical features8,15,16. Here, KRAS is linked to Patent ductus arteriosus.