Although the inflammatory factors such as TNF‐α and IL‐1β are produced in peripheral inflammation areas where they could not pass through blood brain barrier, they could get access to the central nervous system via some unique mechanisms (Banks, 2005; Goehler et al., 2000; Turrin & Rivest, 2004) and contribute to the synthesis of cytokines in central nervous system, thus activating hypothalamus and other brain regions to participate in the pathogenesis of depression. This evidence concerns the gene TNF and depressive symptom measurement.