Binding of β2GPI:aPL on endothelial cells disrupts NO production, leading to increased oxidative stress, and activation of endothelial cells, neutrophils and platelets with formation of neutrophil extracellular traps (NETS) and tissue factor rich microparticles.11 Furthermore, platelet-monocyte aggregates form, which express tissue factor and activate coagulation.8,9,12 Other postulated mechanisms for APS include aPL-induced resistance to activated protein C and downregulation of tissue factor pathway inhibitor.9 Here, F3 is linked to autoimmune polyendocrinopathy.