The activation of the NF‐κB signal cascade in experimental diabetic neuropathy increases the expression of NF‐κB, IκB‐α, and phosphorylated IκB‐α and the nuclear translocation of the p65/p50 subunit, promoting the production of proinflammatory cytokines such as IL‐6, TNF‐α, cox‐2, and iNOS, which then initiates the neuroinflammatory response.124, 125. Here, NFKB1 is linked to diabetic neuropathy.