Several autoantibodies and immune complexes have been linked to vascular damage and atherosclerosis in SLE; as such, antiphospholipid (aPL) antibodies—including lupus anticoagulant, anticardiolipin, and anti-β2-glycoprotein I antibodies (anti-β-2GP1)—are associated with thrombotic events driven by immune-mediated mechanisms [45,46,47]. This evidence concerns the gene APOH and systemic lupus erythematosus.