Furthermore, our data are consistent with four independently generated C9orf72 knock-out mice and one knockout zebrafish model, none of which display any motor or neurodegenerative changes, arguing against haploinsufficiency as a major contributor to C9orf72 ALS/FTD [1, 13, 17, 35], (Schmid, Hruscha, Haass, unpublished). The gene discussed is C9orf72; the disease is amyotrophic lateral sclerosis.