Indeed, anti-β2-GPI antibodies are considered not only a serological marker of APS, but are directly involved in the pathogenesis of thrombosis, since they may interact with ECs and subsequently trigger an up-regulation of Tissue Factor (TF), the major initiator of the clotting cascade, inducing a procoagulant endothelial phenotype [10,11,12]. This evidence concerns the gene F3 and autoimmune polyendocrinopathy.