Earlier work from our lab showed that dysregulation of inhibitory V1 interneurons precedes the degeneration of excitatory V2a interneurons and motoneurons and that stabilizing V1-motoneuron connections improved motor function and saved motoneurons in the SOD1<sup>G93A</sup> ALS mouse model. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.