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. The gene discussed is CCL11; the disease is amyotrophic lateral sclerosis.