The terminal protein of the complement system, complement component 5 (C5), has been identified as a potential therapeutic target in ALS on the basis of evidence of C5a receptor upregulation in post-mortem ALS tissue and SOD1G93A animal models and the fact that pharmacological inhibition of the C5a receptor improved symptoms and prolonged survival in SOD1G93A mice85,86. The gene discussed is C5; the disease is amyotrophic lateral sclerosis.