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). This evidence concerns the gene IDO1 and depressive symptom measurement.