The transfer of mutated ataxin-3 into the nucleus could also be related to altered levels of Trim28 (log2 FC 0.94 in the cerebellum, log2 FC 1.59 in the cerebral cortex), which was shown to drive the nuclear accumulation of two distinct proteins: α-Syn and Tau implicated in Parkinson disease and Alzheimer disease, respectively [68]. Here, TRIM28 is linked to Parkinson disease.