Numerous studies have reported that elevated levels of constitutively expressed HspB1 and HspB5 are observed in pathological cells in which protein folding homeostasis is impaired by the accumulation of pathological proteins that are prone to aggregate, such as α-synuclein, β-amyloid peptide as well as polyQ mutants of huntingtin polypeptide that are responsive of Parkinson's, Alzheimer's and huntington, neurodegenerative diseases, respectively. This evidence concerns the gene HSPB1 and Parkinson disease.