We also postulate that improvements in endothelial dysfunction caused by sustained PPARγ activation in diabetes as well as in other disorders associated with endothelial dysfunction may be related to direct effects of PPARγ activation on endothelial nitric oxide synthase activity [39] mediated by TZD-induced alterations in post-translational mechanisms regulating eNOS activity [40]. This evidence concerns the gene NOS3 and diabetes mellitus.