Thus, could the expression of the non-functional or aberrant form of SOD1 and SOD2 be corrected to reduce ROS and its associated pathology in some patients?, Or could the reinstatement with exogenous functional SOD1 further enhance current treatment for familial amyotrophic lateral sclerosis patients and the administration of SOD2 therapy may reduce OS in motor neuron disease generally? The gene discussed is SOD1; the disease is familial amyotrophic lateral sclerosis.