Although preliminary, this observation is consistent with the hypothesis that hNSCs ameliorate the pathogenic surroundings of MNs, in fact it is now well established that misfolded SOD1 accumulation is a key element of SOD1-mediated ALS, and that the reduction of its level determines significant beneficial effects in preclinical model47,48. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.