Although previous preclinical studies have shown an association between complement pathway activation and increased production of ROS (2, 140, 150), there is a lack of mechanistic understanding of how complement end products such as MAC and the anaphylatoxins, C3a and C5a, produce ROS and the types of ROS involved, especially in the context of diabetes and DKD. This evidence concerns the gene C5AR1 and diabetes mellitus.