It has been confirmed that the IDO1–Kyn–ligand-activated transcription factor (AhR) pathway in thyroid cancer cells would facilitate epithelial-to-mesenchymal transition (EMT) (56), while Kyn depletion in vivo would reverse IDO1-mediated cancer immune suppression in an animal model (57). The gene discussed is AHR; the disease is thyroid gland carcinoma.