Thus, ischemic reperfusion and injury in an experimental model of STZ-induced DM led to the overproduction of NF-κB from endothelial cells and Schwann cells from the sciatic nerve followed by the increased expression of ICAM-1 with the excessive infiltration of monocytes and macrophages, suggesting that NF-κB has a role in mediating the increased inflammatory response at the nerve level in DM [56]. This evidence concerns the gene NFKB1 and diabetes mellitus.