Moreover, mutant SOD1 expressing rodents also recapitulate a salient feature of clinical cases of ALS caused by SOD1 mutations; even though the mutant SOD1 is expressed ubiquitously and persistently from birth, the ALS-like phenotype only presents relatively late in the animals’ life and is the result of selective degeneration of motor neurons in the CNS3, 4. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.