Increased activity and number of glial cells may contribute to neuropathic pain, since activation of glial cells due to neuropathy observed after peripheral nerve damage leads to the release of cytokines, such as TNF-α, IL-6, IL-10, and IL-1β and chemokines at the CNS [50,51], which can modulate inflammatory response and nociceptive transmission [1,52]. The gene discussed is IL1B; the disease is neuropathy.