Notably, PSMB3 may be involved in trinucleotide repeat expansion—a phenomenon seen in several hereditary neurologic disorders (in particular autosomal dominant ataxias)—and it may be driving the trinucleotide expansion process.34 Supporting this hypothesis, there is considerable clinical overlap between MSA and several hereditary ataxias.35,36 Similarly, ribosomal dysfunction with aberrant protein synthesis may promote neurodegeneration.37 Interestingly, no alteration in expression of MAPT—the most obvious candidate gene in the chromosome 17 locus—was found. This evidence concerns the gene MAPT and Rare hereditary ataxia.