The mechanism that links the presence of aPL antibodies to endothelial injury in SLE is not completely clear; possible pathways include anti-β2-GPI binding to β2-GPI and subsequent endothelial cell activation, and the enhanced formation of foam cells induced by ox-LDL/β2-GPI/anti-β2-GPI immune complex formation [45,48]. Here, APOH is linked to systemic lupus erythematosus.