This was based on the key contribution of NOX activity to the rise of reactive oxygen species (ROS) and vascular pathophysiology [21,45] and on the fact that the upregulation of NOX2 has been proposed to participate in vascular alterations in different vascular beds from animal models of diet-induced obesity [46,47,48]. This evidence concerns the gene CYBB and obesity due to melanocortin 4 receptor deficiency.