In GEMM, the initiation and progression of PDA are driven by pancreatic epithelial-specific mutations of the KRAS oncogene and the TP53 tumor-suppressor gene (KrasG12D:Trp53R172H:Pdx1-Cre), referred to as KPC, and resemble key features of human PDA including a dense stroma [53,54]. This evidence concerns the gene PDX1 and Patent ductus arteriosus.