On the other hand, NOX2 is a critical ROS source in endothelial cells and an important regulator of their function, as its genetic deficiency, i.e., the loss of gp91phox expression, leads to the chronic granulomatous disease causing enhanced endothelium-dependent vasorelaxation, the reduction of vascular aging markers and oxidative stress by limiting NO bioavailability [130], whilst NOX5 is actively involved in ROS-mediated proliferation and the formation of capillary-like structures in human microvascular endothelial cells [131]. The gene discussed is CYBB; the disease is chronic granulomatous disease.