While mechanistic insights into the reduced efflux of cholesterol from mouse J774 macrophages to HDLs under conditions that favour nonenzymatic glycation have focussed on apoA-I [71], extensive post-translational modification to other components of the HDL proteome, including deamidation and carbonylation and impaired lipid binding capacity may also contribute significantly to the loss of HDL function in diabetes [71,99,111,112]. Here, APOA1 is linked to diabetes mellitus.