The potential for wild‐type SOD1 dysfunction to contribute to sporadic ALS aetiology is less clear; SOD1 activity is unchanged in red blood cell lysates[178] and post‐mortem frontal cortex[179] of sporadic ALS patients, although to our knowledge activity levels have not been quantified in regions of the spinal cord or brain exhibiting severe motor neuron degeneration in sporadic ALS, with such investigations warranted. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.