TDO-dependent production of Kyn in gliomas has been implied to be a novel mechanism for suppressing antitumor immunity, and supporting tumor growth and motility through activation of the aryl hydrocarbon receptor (AhR).13 As isozymes of TDO, IDO1 and IDO2 are of great interest to determine whether they are involved in the pathological process of gliomas and contribute to the release of Kyn and the activation of the AhR in gliomas. The gene discussed is IDO1; the disease is neoplasm.