Furthermore, while COX‐1−/− offspring showed little or no PDA phenotype, the deletion of one COX‐1 allele increased the penetrance of the COX‐2−/− PDA phenotype such that COX‐1−/+;COX‐2−/− mice had 79% penetrance and COX‐1−/−;COX‐2−/− mice displayed 100% penetrance.55 The gene discussed is PTGS2; the disease is Patent ductus arteriosus.