We thus suggest that blockade of NOX2 per se does not improve the ALS phenotype in SOD1-G93A mice, in accordance with a previous failure to achieve a positive effect on ALS disease progression through the use of specific NOX2 inhibitors (Trumbull et al., 2012), even though NOX2 plays a well-recognized role in ALS pathogenesis (Marden et al., 2007). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.