FASLG and autoimmune polyendocrinopathy: In in vitro models of thrombotic APS, HCQ has been demonstrated to inhibit GPIIb/IIIa expression on aPL-activated platelets [56], to reverse the formation of aPL-β2GPI-PL bilayer complexes [57] and to prevent the aPL-induced disruption of the Annexin A5 shield [58].