Furthermore, APS can be distinct in Primary or Secondary, depending on if it is associated or not with another autoimmune disease [3,4].Anti-β2-GPI antibodies are not only a serological marker of APS but also contribute to the pathogenesis of thrombosis, since they trigger an up-regulation of Tissue Factor (TF) in endothelial cells, the major initiator of the clotting cascade, thereby inducing a procoagulant phenotype [5,6,7]. Here, APOH is linked to autoimmune polyendocrinopathy.