Specifically, in CAD, alterations in HDL3 composition, which include decreases in cholesteryl esters, apoA-I, and paraoxonase 1 (PON1) together with increases in triglyceride and serum amyloid A (SAA) and covalent modifications of HDL-C by oxidation and/or glycation, cause a decrease in cellular cholesterol capacity as well as decreases in the antioxidative and anti-inflammatory activities of these particles. The gene discussed is PON1; the disease is coronary artery disorder.