As an autocrine AhR-IL-6-STAT3 signaling loop sustained the expression of IDO1 in tumor cells fuelled by Kyn that acts as an AhR agonist (25), we analyzed IDO1 gene transcription in the cancer cell lines exposed to the three catalytic inhibitors, and we observed that none of the inhibitors significantly induced the IDO1 gene expression in any of the cell lines (Figure 1C), excluding a transcriptional mechanism involved in the increased IDO1 protein expression by catalytic inhibitors. The gene discussed is AHR; the disease is cancer.