Our data from the current study support the notion that at least one reason for the common failure of IFNα therapy in treatment of human disease is due to its further induction of IDO1, which is already upregulated in RCC as evidenced by such high levels of immunosuppressive kynurenine pathway metabolites that they appear in the urine of RCC patients [8]. The gene discussed is IFNA2; the disease is renal cell carcinoma.