LDLR and atherosclerosis: Previous work demonstrated that AAA-1 could increase intracellular esterified lipid pools by increasing LDL uptake, stimulating the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCoR), the LDL receptor, and by decreasing passive diffusion in macrophages to generate foam cells, the hallmark of atherosclerosis [12, 14].