In ALS mouse models with mutant Cu/Zn superoxide dismutase (SOD1), both beneficial (so-called M2 microglia, regulatory T cells, and Th2 cells) and deleterious (so-called M1 microglia and Th1 cells) immune responses can influence disease progression.27 We showed that IL-10 elevation was correlated with milder symptoms and that IL-4 and eotaxin/CCL11 elevation was correlated with slower disease progression in patients with ALS, suggesting that those cytokines may confer neuroprotection against ALS. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.