The mechanisms of thrombus formation in hyperhomocysteinemia are poorly understood but proposed mechanisms include a homocysteine-mediated enhanced platelet activation; decreased expression of the anticoagulant protein thrombomodulin, which is essential for activation of anticoagulant protein C, and a relative lack of endothelium-derived nitric oxide (NO) leading to endothelial dysfunction.16 This evidence concerns the gene THBD and endothelial dysfunction.