Moreover, upon local lentiviral-mediated expression of the autophagic protein 6/beclin-1 (Atg6/beclin-1) in the brain, we observed an alleviation of neuropathological and behavioral defects of MJD mouse models, evidencing that autophagy activation is a promising strategy to block MJD progression [8, 11]. This evidence concerns the gene BECN1 and Spinocerebellar ataxia type 3.