Although the molecular mechanisms remain elusive, HD pathogenesis have been proposed to be associated with a combination of toxic gain of function of the mutant HTT (mHTT) protein and loss of function of the wild-type HTT protein, untranslated RNA toxicity2, rising instability and oxidative damage of genomic DNA3 and CAG repeat associated non-ATG translation4, where the impaired systems include mitochondrial function, axonal transport, hormone secretion and neurotrophic support5,6. The gene discussed is HTT; the disease is Huntington disease.