Analysis of spinal cord tissue collected from animals at the mid-symptom age of 175–195 days revealed accumulation of iron, loss of ferroxidase activity, and altered expression of iron handling genes (Fig. 5a-d; Supplementary Fig. 9a), indicating disrupted iron homeostasis remarkably similar to human ALS-afflicted tissue (Fig. 1a-e). The gene discussed is CP; the disease is amyotrophic lateral sclerosis.