KRAS and Patent ductus arteriosus: PDA initiates with activating mutation of oncogenes such as KRAS (mutant in over 90% of tumors, and present in the majority of precursor lesions as well) (19) and followed by inactivation of tumor suppressors such as CDKN2A or P53 (altered in 90% and 70% of PDAs, respectively) (20–23).