For example, Huntington’s disease (HD) and spinocerebellar ataxia type 1 (SCA1) are linked to the expansion of the CAG (Cytosine, adenine, guanine) repeat of the huntingtin (HTT) and ataxin 1 (ATXN1) genes, respectively, results in proteins with an unusually long polyglutamine (polyQ) tract that is highly prone to aggregation and causing intracellular deposits in striatal neurons [72,73]. The gene discussed is ATXN1; the disease is juvenile Huntington disease.