Concomitantly, hyperglycemia-induced advanced glycation end products (AGEs) formation and their engagement with renal receptors for AGEs amplify inflammation and fibrosis through diverse intracellular signaling molecules including protein kinase C, transforming growth factor-β and nuclear factor-κB (NF-κB) (16, 17). The gene discussed is NFKB1; the disease is Hyperglycemia.