Based on the studies outlined above, we hypothesize that in situ autoantibody (e.g., aPL)-mediated activation of the complement system generates C4d that can bind to platelet surfaces, and predispose platelets to a pro-thrombotic and pro-coagulating state, thereby promoting the development of thrombotic complications in patients with SLE. Here, FASLG is linked to systemic lupus erythematosus.