While the role of HSP40 and HSP105 in muscle atrophy is not clear, several studies showed that these heat shock proteins can suppress the aggregation of truncated proteins with expanded CAG repeats and cell toxicity in neurodegenerative diseases likely by increasing in target protein degradation via the ubiquitin-proteasome system [61–63]. The gene discussed is HSPH1; the disease is neurodegenerative disease.