TP53 and Patent ductus arteriosus: Mice expressing KrasG12D in the context of double heterozygosity for p53 and p16Ink4a or heterozygosity for p19Arf and p16Ink4a in the pancreas exhibited longer latency and higher propensity for metastasis relative to mice that express KrasG12D in the context of the homozygous deletion of p53 or p16Ink4a/p19Arf separately, highlighting the cooperative role for double heterozygous p16Ink4a and p19Arf-p53 in PDA progression [123].