Todorova et al[4] described that hypercoagulation in APS is closely associated with the protein C/S pathway, in which anti-phospholipid antibodies have the potential to inhibit the anti-coagulation function of protein C. In addition, they also showed that the APS patients had acquired protein C and S deficiency by showing that β2-glycoprotein-I (β2GPI) can inhibit the anticoagulation activity of protein S. This evidence concerns the gene APOH and autoimmune polyendocrinopathy.