There is accumulating evidence for a role of neuroinflammation in ALS pathogenesis, with astrocytes, microglia and T cells actively contributing to neurodegeneration and disease progression in ALS.[11–16] Specifically, reduced expression of mutant superoxide dismutase one (SOD1) protein in microglia[17] and astrocytes[18] has been associated with a slower rate of disease progression. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.