reported associations between higher baseline FXI levels and post‐thrombotic syndrome, venous thromboembolism recurrence, and venous ulcers, which may be attributed to enhanced inflammation and prothrombotic fibrin clot characteristics.[19] Notably, no deep‐vein thrombosis cases were observed in an FXI‐deficient cohort, a rate significantly lower than that in population‐based studies.[20] These findings suggest a potentially critical role for FXI in BD vasculitis pathogenesis, warranting further functional validation. This evidence concerns the gene F11 and Behcet disease.