As it has been shown that inhibition of IDO1 leads to increased AHR activity [33] which in turn induces the expression of IDO2 and/or TDO2 [34], a possible explanation for the failure of IDO1-targeted therapy in cancer is an induction of AHR activity by the inhibitor, even if Kyn formation is sufficiently blocked. The gene discussed is TDO2; the disease is cancer.