Recent preclinical investigations have provided compelling evidence that EA can effectively reduce spinal microglial activation and attenuate the production of pro-inflammatory cytokines such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in animal models of neuropathic pain [20,21]. This evidence concerns the gene IL6 and neuropathic pain.