Although some studies have pointed that elevated and not physiological levels of SOD1WT may cause the neurodegeneration and disease onset in the SOD1 ALS mouse model (Wang et al., 2009; Afshar et al., 2017), the transduction process of WT and mutant hSOD1 in our cellular model did not cause any loss of cell viability. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.