Further, Harmuth et al. [17] reported a decrease in polyubiquitination of VDAC1 and failure of parkin recruitment to depolarized mitochondria in immortalized fibroblast cell lines derived from SCA3 patients, therefore proving the occurrence of parkin-independent mitophagy in the pathogenesis of the disease. This evidence concerns the gene PRKN and Spinocerebellar ataxia type 3.