Experimental studies in neuropathic pain models suggest that tDCS exerts anti-inflammatory and neuroprotective effects, including the down-regulation of pro-inflammatory cytokines (e.g., TNF-α, IL-1β), the up-regulation of IL-10, and the suppression of microglial and astrocytic activation, thereby fostering adaptive plasticity and reducing hypersensitivity (85, 86). This evidence concerns the gene IL1B and neuropathic pain.