The increased damage to motor neurons that accompanies the progression of ALS leads to a transition from a neuroprotective response to an injurious action of neuroinflammation associated to an up-regulation of several chemokines, reactive oxygen species and pro-inflammatory cytokines, such as interferon-γ (IFN-γ), IL-1β, IL-6 and TNFα [28,29,65,66]. The gene discussed is TNF; the disease is amyotrophic lateral sclerosis.