Increasing evidence supports that oxidative stress may play a critical role in the pathogenesis of ALS, the SOD1 protein is an important anti-oxidative enzyme in cytoplasm, and the ALS mutant TDP-43 and FUS cytoplasmic inclusions also co-localize with stress granule in vitro (5, 6). This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.