These effects are accompanied by elevation of serotonergic and noradrenergic activity in the central amygdaloid nucleus, together with increased baseline plasma corticosterone, decreased neurogenesis in the hippocampus and decreased levels of nerve growth factors in the PFC, indicating that IFN-γ modulates anxiety and depressive states and is involved in CNS plasticity (130–132). The gene discussed is IFNG; the disease is Anxiety.