Tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), and high concentrations of pro-inflammatory cytokines in interleukins (ILs) lead to increased inflammatory response, immune imbalance, impact on neuroendocrine function and neurotransmitter metabolism, ultimately resulting in depression (Su et al., 2012). The gene discussed is TNF; the disease is depressive symptom measurement.