The possible roles of antiphospholipid (aPL) in the pathogenesis of thrombosis in APS are well established in the scientific literature, including changes in the coagulation cascade, including inhibition of protein molecules C, antithrombin, and annexin, platelet activation and complement, and increased expression of endothelial adhesion molecules [3]. This evidence concerns the gene FASLG and autoimmune polyendocrinopathy.