It has been well-established that IDO1 plays an important role in the etiology of depression through two mechanisms (6, 12), one is that the overactivated IDO1, an initial and key rate-limiting enzyme of the tryptophan catabolite pathway, tends to direct tryptophan down the kynurenine pathway that releases quinolinic acid, a powerful N-methyl-D-aspartate (NMDA) receptor agonist with definite neurotoxic effects which is involved in the onset of depression (13, 14), and the other is that IDO1 shunts tryptophan from the serotonin synthesis route, thereby favoring depression (15). The gene discussed is IDO1; the disease is major depressive disorder.