To investigate the possible operation of a common pathway triggered by the dysfunction of RBPs that are genetically and pathologically associated with ALS, we first generated SH-SY5Y human neuroblastoma cell lines deficient in either TDP-43, MATR3, FUS, or hnRNPA1 with the use of the CRISPR/Cas9 system (Appendix Fig. S1A–D). The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.