MiR-25 reduces mutant ATXN3 protein levels by interacting with the 3′-UTR of the ATXN3 mRNA, thereby decreasing early apoptosis, increasing cell viability and alleviating the accumulation of mutant ATXN3 protein aggregates in SCA3/MJD cells (Huang et al., 2014). This evidence concerns the gene ATXN3 and Spinocerebellar ataxia type 3.