Arguably, the slow progression of neurologic disease, spanning for clinical onset at 5–6 months of age to progression over another 10–12 months, and the specific clinical features of the disease in G59S-DCTN1 tg mice (see Supplementary Videos) better mirror human ALS than the more commonly used tg SOD1 mouse models [34]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.