Given that both neuroinflammation and neuronal excitotoxicity have been shown to play important roles in neuronal death and promote ALS progression27–31, it is plausible that inhibition of EphA4 function may decrease neuroinflammation32–34 and neuronal excitotoxicity induced by glutamate35. The gene discussed is EPHA4; the disease is amyotrophic lateral sclerosis.