Interestingly, previous studies have shown that Zucker diabetic rats generate ROS by activating NOX,47 and that deletion of the NOX-2 gene protects mice from high-fat diet induced T2D.46 Given the relationship between mitochondrial fission and T2D,21 our findings suggest that NOX-2-derived ROS might play a role in obesity-induced T2D by triggering mitochondrial fission. This evidence concerns the gene CYBB and obesity due to melanocortin 4 receptor deficiency.