The SLE-specific mechanisms associated with chronic inflammation could also contribute to dysregulated lipid signatures, where previous studies have suggested that HDL may be reduced in SLE through inflammatory damage of hepatic cells, as suggested by HDL correlation with liver damage serology [18], elevated levels of autoantibodies against ApoA1 [33], impaired cellular efflux of cholesterol to ApoA1 (HDL) [34], and HDL antioxidant capacity [35]. The gene discussed is APOA1; the disease is systemic lupus erythematosus.