PDA has a complex genomic landscape, and is frequently associated with alterations in a core set of genes, such as activating mutations of the KRAS oncogene (found in >90% of PDA) and inactivation of tumour suppressor genes (TP53, p16/CDKN2A, and SMAD4) [13]. The gene discussed is TP53; the disease is Patent ductus arteriosus.