Multiple lipid defects have been described in JSLE/SLE, including dyslipidaemia comprising elevated levels of triglycerides and LDL, depressed levels of HDL and apolipoprotein-A1 (Apo-A1), and an increased abundance of dysfunctional proinflammatory HDL, lacking the antioxidant capacity of conventionally cardioprotective HDL [6,10,11]. This evidence concerns the gene APOA1 and inherited lipid metabolism disorder.