,5 PDA harbors mutational activation in KRAS and inactivation of CDKN2A, TP53, and SMAD4. 6, 7, 8 Although the molecular basis of PDA is well investigated, the management of PDA remains a huge clinical challenge, including early identification and diagnosis, anticipation of therapeutic responsiveness, and forecasting of outcomes. This evidence concerns the gene TP53 and Patent ductus arteriosus.