In a streptozotocin (STZ)-induced diabetic model, ischemia-reperfusion injury triggered overexpression of NF-κB in the Schwann cells and the diabetes-induced activation of sciatic nerve endothelial cells, along with the subsequent elevated level of ICAM-1 expression and the infiltration of monocyte macrophages as compared to controls, which further indicates that the NF-κB activation mediated the rise in the level of inflammation in diabetic nerves [82]. The gene discussed is NFKB1; the disease is diabetes mellitus.