Studies on murine models of APS have shown that C3 and C5 complement components are crucial for mediating aPL-induced thrombosis in mice [31]; in humans, the placenta from OAPS women exhibited high levels of C4a and C3b deposition, which indicated the possibility of complement activation in the pathogenesis of pregnancy complications in OAPS women [32]. The gene discussed is C3; the disease is autoimmune polyendocrinopathy.