Such abnormal development could contribute to the axonal and behavioral changes we observed and may explain why motor axonopathies have not been previously reported to occur in transgenic SOD1 zebrafish models.37,40,42 To prevent developmental abnormalities from occurring, the amount of human SOD1 mRNA injected, and human SOD1 protein expressed, was kept at a lower level than in a previously reported transient SOD1 zebrafish model.35 Furthermore, we were careful to only study animals with normal gross morphology (body shape and length), to limit the effect of developmental delay. This evidence concerns the gene SOD1 and Global developmental delay.