In fact, previous studies showed that expression of Nogo-A, a Nogo isoform, was enhanced in the muscles of ALS patients [15], and genetic deletion of Nogo-A in ALS model mice harboring a mutant human superoxide dismutase 1 (SOD1) transgene prolonged lifespan, suppressed muscle denervation, increased motor neuronal survival, and reduced the number of ubiquitinated inclusions [12]. Here, SOD1 is linked to amyotrophic lateral sclerosis.