Different explanations can be considered with regard to this finding confirmed by the existing literature [71]: (1) MCP-1 may exert a protective role on mood disorders, balancing monoamine neurotransmission that results in altered depression [72]; (2) MCP-1 could induce a pro-inflammatory state and have a secondary role in the long term [73]; and (3) MCP-1 could accumulate in tissues where it exerts its chemoattractant and pro-inflammatory actions, resulting in a decrease in the plasma of patients with depression [74]. This evidence concerns the gene CCL2 and mood disorder.