Activated platelets and coagulation factors drive recruitment of neutrophils and monocytes, generating interleukin-6 (IL-6), tumor necrosis factor-α, and reactive oxygen species. Chronic inflammation accompanying these rheumatologic diseases is considered to increase the risk of venous thromboembolism by up-regulating procoagulants, down-regulating anti-coagulants, suppressing fibrinolysis, and causing endothelial dysfunction [11]. This evidence concerns the gene TNF and venous thromboembolism.