In this case, the patient was a middle-aged male with a history of congenital heart disease in which arterial ductus arteriosus caused sustained high flow and pressure at the main pulmonary artery junction, and finally pulmonary artery endothelial cell damage, which impaired the antithrombotic function of the arterial wall by down-regulating the endothelial nitric oxide synthase (eNOS) or stimulating the expression of the adhesion receptor (8, 13), and, thus, formation of an in situ thrombus at the junction out of the main pulmonary artery. The gene discussed is NOS3; the disease is congenital heart disease.