In particular, the upregulation of the chaperone HSPB8, or of its Drosophila melanogaster homolog (HSP67Bc) was shown to protect against protein aggregation and toxicity in cell and fly models of ALS and polyglutamine diseases and cooperation between HSPB5 and the mammalian disaggregase machinery was very effective in dissolving protein aggregates (Carra et al., 2010; Duennwald et al., 2012; Crippa et al., 2016). The gene discussed is CRYAB; the disease is amyotrophic lateral sclerosis.