Indeed, this review has presented evidence that complement end products such as MAC and the anaphylatoxins C3a and C5a are activated in diabetes, with NOX4 as a key source of ROS responsible for renal injury in diabetes (71); it would not be surprising if the complement probably plays a role in promoting oxidative stress and renal injury in DKD through the actions of NOX isoforms. This evidence concerns the gene C5 and diabetic kidney disease.