While our proteomics analysis did not detect a significant difference in HDL-associated apoA-I levels between T2D and controls, other investigators have suggested that hyperglycemia results in nonenzymatic glycation of apoA-I[37] and that glycation of apoA-I, and advanced glycation end-products (AGEs) in general, may contribute to reduction of HDL ability to activate eNOS.[47] Although the T2D patients had elevated glucose and glycated HbA1c, the concentrations we observed only slightly correlated with the ability of HDL to activate eNOS. Here, APOA1 is linked to type 2 diabetes mellitus.