With regard to this idea, amply evidence indicates that NO and O•−2 are produced by ALS glial cells—as a result of either mitochondrial dysfunction, increased NADPH oxidase activity, or inflammation—and play a pivotal role in motoneuron pathology and death (Carter et al., 2009; Drechsel et al., 2012). The gene discussed is FMO5; the disease is amyotrophic lateral sclerosis.