Additionally, NSCLC adenocarcinoma cells that could secrete large amounts of mucin which could promote vascular endothelial degeneration and epithelial cell shedding, leading to localized thrombus formation.11,12 Furthermore, NSCLC cells might release tissue factor and prothrombin activators, which might promote blood coagulation and increase the likelihood of thrombus formation.13 In the advanced NSCLC, levels of thrombin and procoagulants were higher, which increased plasminogen activator inhibitor-1, contributing to a greater risk of thrombus formation. The gene discussed is F3; the disease is adenocarcinoma.