One may speculate that the improved insulin sensitivity could potentially be due to the transfer of apoC-III from lipoproteins in VLDL- and LDL-density classes to lipoprotein subclasses in HDL, since it has been demonstrated that the plasma concentration of apoC-III bound to apoB-containing lipoproteins strongly correlates with the degree of insulin resistance in subjects with the metabolic syndrome [24]. The gene discussed is APOB; the disease is Insulin resistance.