Based on the aforementioned evidence, we hypothesised that EA treatment at GB20/GB34 would alleviate pain hypersensitivity in a rat model of migraine by ameliorating neuroinflammation via the inhibition of microglia and a decrease in microglial-mediated inflammatory cytokines (IL-1β, TNF-α and IL-6), and that microglial activation and relevant inflammatory responses might be regulated by microglial TLR4 and the downstream molecule NF-κB. This evidence concerns the gene NFKB1 and migraine disorder.