TERT and coronary artery disorder: We recently showed that in atrial vessels from human subjects with CAD, the increase in mitochondrial ROS (mtROS) altered endothelial function and reduced the bioavailability of nitric oxide (13, 14); the increase in TERT can modulate cellular redox state by upregulation of mitochondrial antioxidant enzymes (15), reduce mtROS production (16) and reverse the impaired phenotype observed in coronary vessels from CAD human subjects (6).