These behaviors are underlined by (a) increased serotonergic and noradrenergic activity (i.e., greater metabolite accumulation) in the central amygdaloid nucleus, together with (b) increased baseline plasma corticosterone, (c) decreased neurogenesis in the hippocampus, and (d) decreased levels of nerve-growth factor in the prefrontal cortex, suggesting that IFNG modulates anxiety and depressive states and is involved in CNS plasticity [264, 265]. The gene discussed is IFNG; the disease is Anxiety.