Given that the level of ADAR2 reduction is more modest in the motor neurons of patients with sporadic ALS (Hideyama et al, 2012; Kawahara et al, 2004) compared to the AHCs of AR2 mice in which ADAR2 is absent (Hideyama et al, 2010), a therapeutic level of ADAR2 activity would be more easily achieved in ALS patients using this method of gene delivery. This evidence concerns the gene ADARB1 and amyotrophic lateral sclerosis.