However, mice with C9orf72 deficiency, or those expressing loss-of-function mutations, develop immune defects, increased expression of inflammatory cytokines, and autoimmunity [98,99], but no neurodegenerative phenotype, arguing against haploinsufficiency as a single causative factor in ALS/FTD. This evidence concerns the gene C9orf72 and amyotrophic lateral sclerosis.