However, wild-type SOD1-expressing mice have nonetheless provided some evidence to implicate a role for SOD1 in cases of ALS that do not involve mutant SOD1; subtle phenotype changes have been reported for hemizygous, wild-type SOD1-overexpressing mice at a relatively young age [15], whereas a more recent study has described pronounced ALS-like features in homozygous, wild-type SOD1-overexpressing mice [16]. Here, SOD1 is linked to amyotrophic lateral sclerosis.