Our finding is in accordance with the fact that Mammen and Bick suggested platelet hyperaggregability in the context of SPS as the cause of thromboembolic events, which could not be explained by any of the established risk factors (Protein C/S deficiency, Factor V Leiden mutation, antiphospholipid syndrome, etc.)[5,6]. This evidence concerns the gene F5 and antiphospholipid syndrome.