Our work does not exclude other—ribosome-independent—mechanisms that may contribute to C9ORF72-ALS/FTD, including: defective nuclear transport31,32, defective splicing20,33, aggregation of non-arginine DPR proteins, such as poly-GA34, repeat-RNA toxicity, or loss of functional C9ORF72 protein, etc. (as reviewed in refs. 7,35). This evidence concerns the gene C9orf72 and amyotrophic lateral sclerosis.