Over the past few decades, along with identifying the HTT gene, considerable progress has been made in learning the mechanism of neurodegeneration caused by mutHTT, including increased excitotoxicity injury in neurons through a deficiency of wild-type HTT [4], nutritional support disorders from neurons [5], the appearance of inclusion bodies derived from aberrant protein accumulation and the influence of polyglutamine length on the extent of mutHTT aggregates [6], mitochondrial impairment [7], and defective axonal transport in HD neurons [8, 9]. This evidence concerns the gene HTT and Huntington disease.