Importantly, these phenotypes could be rescued with the expression of human C9orf72 mRNA, confirming that they were due to the direct effects of loss-of-function of c9orf72. This zebrafish knockdown model exhibited important motor behavioural defects as observed in the disease, allowing us to think that the loss-of-function has a contribution in ALS pathogenesis, but is not exclusive. Here, C9orf72 is linked to amyotrophic lateral sclerosis.