Because depression is characterized by a desynchronized circadian rhythms of sleep/wake cycle, including HPA axis hyperactivity [36,37], our previous and present findings support the presumption that Pir might be considered an antidepressant candidate in the PNS model with potency to correct circadian rhythm abnormalities, sleep disturbances and HPA axis hyperactivity through activation of MT receptors. The gene discussed is PIR; the disease is depressive symptom measurement.