F3 and autoimmune polyendocrinopathy: The pathogenesis of APS is multifaceted, and a growing body of evidence supports that the development of APS is caused by aPL mediated, interactions between inflammatory and thrombotic mechanisms centered on disruption of coagulation and fibrinolysis, involving aPL-mediated activation of platelets, monocytes and endothelial cells, altered adhesion molecules and activation of pro-inflammatory cytokines, complement and neutrophil activation, and tissue factor upregulation and many others (3, 25, 26).