We found that the ATP7A-M1311V-iNSC population showed no difference in the proliferation rate compared to the control iNSCs, but showed lower cell viability, lower LOX activity, and elevated ROS under basal cell conditions, similar to the results from the experiments with iPS cells described above (Supplementary Fig. 10), supporting our conclusion that the ATP7A M1311V mutation has a potential responsibility for ALS. The gene discussed is ATP7A; the disease is amyotrophic lateral sclerosis.