We used our in vitro ACM-hSOD1G93A model system to investigate the potential causes of c-Abl activation in ALS: in agreement with earlier studies, which report that oxidative stress can induce c-Abl activation (van Etten, 1999; Klein et al., 2011; Schlatterer et al., 2011a), we found that ROS (H2O2) increases c-Abl phosphorylation, and that co-application of antioxidants plus ACM-hSOD1G93A strongly reduce activation of this kinase, in a manner similar to that of the c-Abl inhibitor STI571. This evidence concerns the gene ABL1 and amyotrophic lateral sclerosis.