In contrast to the “second strike” theory of APS thrombosis, OAPS patients exhibit elevated β2GP1 levels in placental endothelial cells, syncytial trophoblasts, and extravillous trophoblasts, resulting in aPL binding without a “second strike” and leading to various mechanisms of adverse pregnancy outcomes, even at low aPL titers [15]. This evidence concerns the gene FASLG and autoimmune polyendocrinopathy.