Furthermore, other mechanisms are described in patients with APS, as HCQ inhibits complement activation, reduces production of tissue factor (TF), disintegrates binding of aß2GP1 to ß2GP1 and complexes of phospholipid bilayers, inhibits production of tumor necrosis factor α (TNFα) in monocytes, restores anticoagulant action of annexin A5, reduces trophoblast alteration, fetal death, placental insufficiency, thrombosis, endothelial dysfunction and decreased LA levels (Table 1). The gene discussed is TNF; the disease is placental insufficiency.