In order to verify whether excessive S-nitrosylation occurred in ALS, we initially performed biotin switch assays of S-nitrosylated proteins (PSNOs) in spinal cord of mice overexpressing the fALS associated G93A mutant form of SOD1 that we selected as in vivo elective model of ALS; Figure 6(a) shows that PSNOs levels were significantly increased in symptomatic G93A mice (135-day-old), confirming the hypothesis that ALS was accompanied by aberrant S-nitrosylation. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.