Even if protein mislocalization, particularly TDP-43 and FUS, plays a key role in ALS pathology (Boeynaems et al., 2016; Dormann and Haass, 2011), in LCLs from sALS patients we did not report nucleus-cytoplasmic transport defects and/or protein aggregation. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.