In addition, pro-inflammatory cytokines such as interferon-gamma (IFNγ), IFNα and tumor necrosis factor (TNFα) contribute to the development of depressive disorder by regulating neuronal excitability, reducing the levels of serotonin and causing changes in other mechanisms of neurotransmission and neuronal signaling in brain regions involved with depression, oxidative injury, and hippocampal neuronal damage [44,45,46]. This evidence concerns the gene IFNG and depressive symptom measurement.