In subsequent studies, genetically halving mGluR1 and mGluR5, or ablating mGluR5, significantly ameliorated disease progression and survival probability in SODG93A mice [308,309,310], and produced a reduction in astrogliosis and microgliosis, always accompanied by positive outcomes for the ALS phenotype. The gene discussed is GRM5; the disease is amyotrophic lateral sclerosis.