The contribution of insulin resistance to pathogenic mechanisms involved in atherosclerotic disorders such as CAD can be biologically plausible; the accumulation of free fatty acids (FFAs), particularly in the hepatic tissue, following a decrease in the sensitivity to insulin (i.e., insulin resistance) and therefore the lack of lipolysis-inhibitory effects of insulin, may result in an elevation in apoB and very low density lipoprotein cholesterol (VLDL-C) formation and reduction of their clearance. The gene discussed is APOB; the disease is coronary artery disorder.