In T2D, hypertensive, and atherosclerotic humans that often suffer from vascular ROS/RNS stress, the levels of endothelial eNOS are actually elevated due to elevated H2O2 overstimulation of its expression, but the enzyme is largely uncoupled, generating damaging ROS/RNS as described above [38,49,50,51,52,69]. This evidence concerns the gene NOS3 and type 2 diabetes mellitus.