Other autoantibodies have been described as contributors of accelerated atherosclerosis in SLE: anti-HDL-IgG that induce LDL to enter the ECs; anti-apolipoprotein A1 (ApoA1)-IgG that activating the transcriptional nuclear factor kappaB (NF-kB) favor the expression of inflammatory factors at endothelial level (46); anti-FXa-IgG can inhibit FX enzyme (47), modifying the of hemostasis/thrombosis equilibrium and promoting ED (48). This evidence concerns the gene APOA1 and atherosclerosis.