Thus, they proposed a thrombogenic mechanism for aPL in which antibodies bind to the complexes of PL and coagulation proteins, including prothrombin, protein S, and protein C. Several studies reported the presence of antiprotein S and/or protein C in APS patients [13, 14], though with less sensitivity and specificity as compared to IgG aCL. The gene discussed is F2; the disease is autoimmune polyendocrinopathy.