FUS accumulation in large cytoplasmic inclusions in ALS-FUS postmortem tissue (13–15), ALS mutations in FUS 3′ untranslated region leading to its overexpression (16), and FUS mRNA up-regulation in physiological cell models of ALS-FUS (17) all point to a disrupted control over its cellular levels as a disease hallmark. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.