Studies in Italy and Lebanon have revealed that the presence of factor V Leiden, prothrombin, and methylene tetrahydrofolate reductase mutations did not contribute to the risk of TEE in patients with thalassemia.30–31 The presence of cardiac, hepatic, or endocrine dysfunction may also contribute to the hypercoagulability in thalassemia.8 This evidence concerns the gene F5 and thalassemia.