Multiple proteolytic cleavage sites create unique splicing patterns in the HTT protein and produce a variety of N-terminal fragments.1,6,7 Moreover, the expanded polyQ tract creates aberrant splicing of the HTT protein that results in the formation of small oligomeric fragments.1,9,11 These oligomeric fragments fold, form aggregates, accumulate in cells, and disrupt cellular functions.1,9,10 Although there is a great advancement in the understanding of HD pathogenesis and the development of drugs and therapeutics, HD remains incurable and the search for effective treatments continues. This evidence concerns the gene HTT and Huntington disease.