We have shown competition between ALS mutant FUS and the translational repressor FMRP for HuD 3′UTR binding, resulting in increased HuD levels, with consequences on HuD targets, NRN1 and GAP43, in turn involved in abnormal axonal morphology and recovery upon injury [15, 21, 25]. Here, FMR1 is linked to amyotrophic lateral sclerosis.