Genetic and molecular analysis of these disorders have revealed that the repeat expansion can result in either a loss of function of the gene (Fragile-X syndrome and Friedreich's ataxia) or a gain of function of the encoded protein (SCA1, SCA2, SCA3, SCA6, SCA7, SCA17, Huntington's disease, DRPLA, and oculopharyngeal muscular dystrophy) [7], [8]. This evidence concerns the gene ATXN3 and juvenile Huntington disease.