These results indicate that while the Y2 receptor of NPY is involved in both the role of NPY in developing HD pathology and in the therapeutic efficacy of NPY, its activation does not restore HD-deficits, indicating a role for other receptors, such as Y1, which has been shown in preclinical PTSD models to be responsible for the therapeutic benefits of IN-NPY [130]. The gene discussed is NPY; the disease is post-traumatic stress disorder.