Abstract: Cancer-associated venous thromboembolic disease (VTE) has become the second leading cause of death among cancer patients. Some scholars have proposed a variety of thrombosis risk models to screen out patients with a higher thrombosis risk and then offer them drug or physical intervention measures to reduce the incidence of cancer-associated VTE. However, with the continuous development of precision medicine, these conclusions can no longer meet the requirements of medical personnel to explore the problems of cancer-associated VTE. Genetic testing has become the "baseline" test in cancer patients. Common driver genes, such as the epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), v-ros UR2 virus oncogene homolog 1 (ROS1), and kirsten ras sarcoma (KRAS), have become the normalcy and are recommended by the guidelines for clinical use. The status of gene mutations in clinical prognosis and treatment is increasingly prominent. This review discusses whether there is a correlation between cancer-associated VTE and gene status and whether we can screen out cancer populations with a higher risk of thrombosis according to gene status, thus providing a theoretical basis for better implementation of prevention management strategies.