This is because, in the astrocytes of transgenic ALS mice, Nrf2 overexpression significantly extended the time of survival, delayed the disease onset and reduced the rate of motor neuron damage [194], while the upregulation of Nrf2 in neurons or in type II skeletal muscle fibers delayed the disease onset but failed to extend survival [195]. The gene discussed is NFE2L2; the disease is amyotrophic lateral sclerosis.