Although we note that the early disease features seen in this zebrafish model (electrophysiological changes and NMJ denervation) are also observed in the presymptomatic rodent models of SOD1-related ALS and to a limited extent in presymptomatic human patients, further work is necessary to determine whether these early changes reflect the initiation of a progressive pathophysiological cascade that eventually culminates in motor neuron loss. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.