Youn et al. (2012) reported that the activation of NOX1 was associated with eNOS uncoupling and endothelial dysfunction in streptozotocin-induced type 1 diabetic mice aorta. Furthermore, Gray et al. (2013) reported that genetic deletion of NOX1 in diabetic mice led to reduced diabetes mellitus symptoms, suggesting a key role of NOX1-derived ROS in diabetes. The gene discussed is NOS3; the disease is endothelial dysfunction.