126). Interestingly, SCA3 can present clinical and neuropathological features of PD and the affected brain regions can overlap (Ref. 127). As mentioned before, Parkin, mutations which are a common cause of PD, acts as an E3 ubiquitin ligase (Ref. 128). Although both ATXN3-WT and ATXN3-PolyQ can deubiquitinate Parkin, the pathological form of ATXN3 promotes the clearance of Parkin via the autophagy pathway, implicating increased Parkin turnover in the pathogenesis of SCA3, possibly explaining some of the Parkinson-like features observed in the disease (Ref. 129). This evidence concerns the gene PRKN and Parkinson disease.