HSPB8 and amyotrophic lateral sclerosis: Indeed, HSPB8 facilitates the degradation of several misfolded proteins (Htt43Q, Androgen Receptors 46Q and 112Q, mutated SOD1, mutated TDP-43, and dipeptide repeat proteins from the C9ORF72 gene containing the expanded G4C2 stretch) responsible for neurodegenerative diseases, such as frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), spinal and bulbar muscular atrophy (SBMA), and Huntington’s disease (HD), and contributes to maintain a normal autophagic flux and to promote neuronal survival [20,23,26,60,66].