Among them, our previously constructed the huntingtin knock-in (HD-KI) pig model was constructed by replacing the sequence in the corresponding site of the pig HTT with the human mutant HTT exon1 carrying abnormal expanded CAG repeat sequence, and model serves as an ideal animal model for studying therapeutic interventions in HD, as it faithfully recapitulates the pathological features and motor deficits observed in HD patients [50]. This evidence concerns the gene HTT and Huntington disease.