Finally, since enhancing the BDNF–CREB activity through pharmacological treatments with various classes of antidepressant drugs or environmental enrichment abolished the alcohol-induced anhedonia and depressive behaviors seen during protracted abstinence (104, 107, 108), supporting the hypothesis that BDNF–CREB signaling pathway may be a potential therapeutic target for interventions in alcoholism–depression coincidence. The gene discussed is BDNF; the disease is depressive symptom measurement.