Preclinical data provide a coherent mechanistic substrate for these translational prospects: decreased Angptl3 expression protects ApoE−/− mice from atherosclerosis (104); antisense inhibition of Angptl3 delays plaque progression while lowering atherogenic lipoproteins and enhancing HDL-mediated RCT (60, 105); and monoclonal antibody blockade reduces TG and non–HDL lipids in mice and primates with endothelial lipase–linked HDL remodeling (106). This evidence concerns the gene LIPG and atherosclerosis.