Given the extraordinary molecular heterogeneity of ALS, we developed a suite of ALS models representing genetically diverse fALS aetiologies in NSC-34 cells by expressing EGFP-/tGFP-/mCherry-fusions of mutant SOD1, TDP-43, FUS, CCNF, UBQLN2, OPTN, VCP or VAPB. This evidence concerns the gene FUS and amyotrophic lateral sclerosis.