Multiple pathological events have been identified in SOD1-ALS mice models, including mitochondrial abnormalities, ER stress, proteotoxic stress, abnormal ion and glutamate homeostasis, abnormal axonal transport, axonal degeneration, and non-cell autonomous toxic events mediated by glial cells, but the relationship between these events, and the extent to which they occur in SOD1-ALS and other ALS patients remains to be established [70]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.