Circulating LDL molecules are transported from the vascular space into the arterial wall and retained in the extracellular matrix, where they are prone to form oxidized LDL that contributes to atherosclerotic plaque formation [62]; therefore, the very early stages of atherosclerosis include the increased arterial entry and retention of LDL because of their decreased clearance by LDL-R in plasma, with increased oxidation of LDL in the arteries and greater endothelial dysfunction, foam cell formation, and the appearance of carotid intima-media thickness as early carotid lesions [62]. This evidence concerns the gene LDLR and atherosclerosis.