Atherogenic dyslipidemia is characterized by high levels of apolipoprotein B (apoB)-containing lipoproteins, including very-low-density lipoprotein (VLDL) and its remnants and small, dense LDL (sdLDL) particles, and reduced levels of high-density lipoprotein cholesterol (HDL-C). Extensive evidence shows that atherogenic dyslipidemia contributes not only to residual macrovascular risk but also to inflammation and microvascular complications. The National Cholesterol Education Program (NCEP) recommended using non-high-density lipoprotein cholesterol (non-HDL-C) to surrogate atherogenic lipoproteins in clinical practice. Elevated non-HDL-C may represent abnormal secretion, abnormal catabolism, and/or abnormal hepatic uptake of triglycerides (TG)-rich lipoproteins. Recently, we have done a pilot study to study the associations between SAH gene variants and atherogenic dyslipidemia (surrogated by non-HDL-C) in postmenopausal women. We found that homozygosity for SAH haplotype 3 was associated with increased adiposity, insulin resistance, and elevated levels of non-HDL-C in the postmenopausal women. Moreover, researchers have identified that there are at least four members in the SAH gene family: SAH, MACS1, MACS2, and MACS3. All of them seem to have acyl-CoA synthetase activity toward medium-chain fatty acids and all are clustered in chromosome 16p12. In the present study, we propose to do a two-year study to examine the associations between the SAH gene family and atherogenic dyslipidemia in postmenopausal women.