When taken with a report that ALS patients with mutations in the 3′ UTR region of FUS accumulate those variants at increased levels in patient fibroblasts (Sabatelli et al., 2013), it is therefore likely that even a modest increase in FUS (human mutant or wild-type) is sufficient to trigger age-dependent motor deficits. The gene discussed is FUS; the disease is amyotrophic lateral sclerosis.