Together, this inflammation induced reduction in HDL levels and the capacity of HDL to carry out its primary atheroprotective functions of reverse cholesterol transport (removal of cholesterol from peripheral tissue) and inhibition of LDL/VLDL (ApoB expressing lipoproteins) oxidation (reducing LDL/VLDL recognition by scavenger receptors), could dramatically increase CVD risk in SLE patients through the increased LDL cholesterol uptake (and reduced lipid efflux) by macrophages in atherosclerotic plaques, coupled with the persistent chronic inflammatory environment of SLE. This evidence concerns the gene APOB and systemic lupus erythematosus.