An example case is a recent report on Huntington’s disease (HD) [85,86], a monogenic, autosomal-dominant trinucleotide CAG-repeat expansion within exon 1 of the HTT gene, resulting in an abnormally long polyglutamine (polyQ) tract of the mutant Huntingtin (mHTT) protein [87,88]. This evidence concerns the gene HTT and Huntington disease.