Pulmonary embolism refers to a syndrome in which various emboli enter the pulmonary circulation and block the pulmonary artery or other branches, causing obstruction of the pulmonary circulation. The clinical symptoms of pulmonary embolism are not typical, some show sudden coughing and difficulty in breathing, some show headache and dizziness, some show “epileptic” seizure, and some show abdominal pain, and some show violent and life-threatening symptoms. Pulmonary embolism is not obvious in the early stage, and the onset is sudden, so it is called the “silent killer”! The diagnosis of pulmonary embolism is no longer difficult, but the key is to raise awareness of the diagnosis and prevention of pulmonary embolism. As we know, pulmonary embolism is often complicated by heart failure, cerebrovascular disease paralysis, pulmonary disease respiratory failure or fracture, which leads to activity limitation or long-term bed rest. However, we have observed in our clinical work that under the same circumstances, some patients have pulmonary embolism complications within days or weeks, while some patients are bedridden for several years or more than ten years without pulmonary embolism. What exactly is the reason? We have to start from easy embolism. Embolism is not a single disease, but a state in which thromboembolism easily occurs due to congenital deficiency of anticoagulant substances or the presence of various acquired causes that lead to damage of blood vessel walls or slow blood flow and hypercoagulable state of blood. Congenital anticoagulant substance deficiency is related to genetic genes, and acquired factors include: 1, diseases such as tumor, varicose veins of lower extremities, intravenous indwelling needle, cardiovascular and cerebrovascular disease long-term bed or sedentary wheelchair, autoimmune diseases, etc. 2, bad living habits such as: sitting in a chair at home traveling in a car, sedentary forgetfulness of mahjong and games, etc. Patients with hereditary factors of thrombosis, together with any or more acquired factors later in life will be prone to pulmonary embolism. If the patient is found to have acquired risk factors, such as: advanced age, absolute bed rest >3 days, obesity. For varicose veins of the lower extremities and autoimmune diseases, the patient should be examined for genetic factors, such as: coagulation factor 5 gene, prothrombin gene, coagulation factor 13 gene, plasma fibrinogen inhibitor-1 gene, methylenetetrahydrofolate reductase gene, folate gene, protein C gene, and thrombomodulin gene. Once thrombosis occurs, the course of anticoagulation should be extended or even lifelong anticoagulation should be given. Therefore, the genetic examination is a good guide to the prevention and treatment of pulmonary embolism.