Research aimed at understanding amyotrophic lateral sclerosis (ALS) has seen exceptional growth in the past few years. New genes, new models, and new mechanisms have not only improved our understanding, but also contributed to the increasing complexity of ALS pathogenesis. The focus of this piece is to highlight some of the more notable developments in the field and to encourage a re-appreciation for the superoxide dismutase 1 (SOD1) mouse models.