In line with this, most of the mechanisms involved in the inflammation-depression -relationship have been described for TNF-α and IFN-γ, but not CRP, including the stimulation of the indolamine-2,3-dioxygenase (IDO) (10), the relationship with the psychopathology of depression (37–39) and the potential as an antidepressant drug target (14, 40). The gene discussed is IFNG; the disease is depressive symptom measurement.