Both central and peripheral inflammation have been well established in ALS, with this pathology encompassing increased levels of inflammatory cytokines including tumour necrosis factor α (TNF-α) and interleukins (IL-1β, IL-4, IL-6 and IL-10) the involvement of non-neuronal cells including activation of microglia and astrocyte dysfunction, and T lymphocyte infiltration into the central nervous system (CNS) [14–17]. The gene discussed is IL1B; the disease is amyotrophic lateral sclerosis.