In NTg mice, HSPB8 is also present at high levels in muscles; instead, in the SOD1-G93A ALS or SBMA AR113Q mouse models, HSPB8 expression is robustly increased paralleling disease progression (Crippa et al., 2013a,b; Rusmini et al., 2015). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.