Incubating HSVECs with AICAR, an artificial, ROS-independent activator of AMPK, known to stimulate the kinase in endothelial cells [19], resulted in a significant increase in AMPK activity in cells from patients with CAD alone but not in cells from those patients with CAD and T2D whose basal AMPK activity approached maximal levels. The gene discussed is PRKAA2; the disease is coronary artery disorder.