In tumor cells, overactive STAT3 reduces the expression levels of immunostimulatory factors, including IFN‐γ and pro‐inflammatory cytokines (IL‐6, IL‐12, and TNF‐α), ultimately promoting the formation of an immunosuppressive TME.[37, 39] Given that AhR is the canonical receptor for KYN, we hypothesized that these nano‐systems would improve the imbalance in KYN metabolism by inhibiting the AhR/STAT3/IL pathway. The gene discussed is AHR; the disease is neoplasm.