C9orf72 and amyotrophic lateral sclerosis: Potential mechanisms implicated in the pathogenesis of c9FTD/ALS include the loss of C9ORF72 protein function, repeat RNA-mediated toxicity, and toxicity from the accumulation of dipeptide repeat (DPR) proteins produced by repeat-associated non-ATG (RAN) translation (reviewed [19, 55, 56]).