Cytokines such as IL-1β, TNF-α and IFN-γ seem to contribute to the pathophysiology of depression by stimulating the hypothalamic-pituitary-adrenocortical axis (Rosenblat et al., 2014), thus activating monoamine reuptake (Raison et al., 2009), and decreasing production of serotonin through increased activity of indoleamine-2,3-dioxygenase (IDO; Müller and Schwarz, 2007). This evidence concerns the gene IL1B and depressive symptom measurement.