Regarding the onset mechanism for IFN-induced depression, it was recently reported that inflammatory cytokines [38] and oxidative stress induced by ROS production [35] were influential and that continuously elevated glucocorticoid concentrations induced by disrupting the negative feedback mechanism in the hypothalamic-pituitary-adrenal axis brought on neuroplasticity of the hippocampus [39]. This evidence concerns the gene IFNA1 and depressive symptom measurement.