In addition, given HDL-SAA is a more stable marker of chronic inflammation than serum-SAA alone [19], and as CVD correlates with HDL subfraction dysfunction [14, 20], we chose to directly measure functional components of HDL in subjects with T2DM, namely, the activities of HDL-PON-1, CETP, and LCAT. This evidence concerns the gene LCAT and type 2 diabetes mellitus.