Indeed, when overexpressed in ALS and SBMA cell models, HSPB8 restores an impaired autophagy flux to normal levels and it enhances the degradation of disease-associated misfolded protein and aggregates of mutant SOD1, two disease-associated fragments of TDP-43 (TDP-35 and TDP-25), the RAN-translated dipeptide repeats of the C9ORF72 G4C2 expansion, and ARpolyQ. Here, HSPB8 is linked to amyotrophic lateral sclerosis.