Mechanistically, our research revealed that, in “cold” solid tumors, the excessive expression of IDO1 derived from tumor cells leads to the accumulation of KYN, which activates interleukin (IL) family signaling through the aryl hydrocarbon receptor/signal transducer and activator of transcription 3 (AhR/STAT3), exerting systemic effects on the malignant progression of tumors and antitumor immune resistance. The gene discussed is AHR; the disease is neoplasm.