The mechanism of action of GLE may be owing to its ability to suppress the hyperglycemia by regulating the secretion of insulin from the pancreatic beta-cells and in turns it may ameliorate the oxidative stress and confirm the availability of enough antioxidant enzymes and it is well known that presence of oxidative stress and inflammation will initiate NF-kB activation; thus GLE alleviated the symptoms of diabetes by a successive regulation of hyperglycemia followed by oxidative stress and NF-kB pathway regulation. This evidence concerns the gene NFKB1 and diabetes mellitus.