Antioxidant supplementation by diosmin suppressed diabetes induced ROS resulting in deactivation of NF-κB associated pro-inflammatory chemokines and cytokines such as macrophage chemotactic protein (MCP-1), tumor necrosis factor (TNF-α), and interleukins (IL-1β and 6) [98]. This evidence concerns the gene NFKB1 and diabetes mellitus.