Using the IN route of administration, Esther Sabban’s group has already demonstrated that IN NPY ameliorates molecular and behavioral alterations in a rodent model of PTSD [10, 11, 14] and others have shown that IN NPY suppresses microglia activation and cerebral TNF-α expression in a transgenic murine model of Huntington’s disease [15]. The gene discussed is TNF; the disease is juvenile Huntington disease.