IL-6 seems to promote atherosclerosis by various metabolic, endocrine, and cellular mechanisms, including increased hepatic synthesis of acute phase reactants, monocyte activation and increased macrophage lipid uptake, lower HDL-cholesterol levels, decreased lipoprotein lipase activity, and activation of the hypothalamic–pituitary–adrenal axis (a potential inducer of obesity, hypertension, and insulin resistance) [40]. This evidence concerns the gene LPL and atherosclerosis.