Recent work has demonstrated that transient mutant human FUSR521H expression resulted in pathological hallmarks of ALS at the zebrafish NMJ, which include reduced fidelity of synaptic transmission, reduced quantal content and abnormal synaptic morphology (Armstrong and Drapeau, 2013b), as for TARDBP. FUS and TDP-43 share some structural similarities, and evidence that they might act in a molecular pathway that is separate from SOD1, with TDP upstream from FUS, has been demonstrated by epistasis analyses in zebrafish (Kabashi et al., 2011a) and in Drosophila (Wang et al., 2011). Here, FUS is linked to amyotrophic lateral sclerosis.