AHR activation in TAMs, driven by GBM-secreted tryptophan metabolites like TDO2 and IDO1, upregulates CCR2 and Krüppel-like factor 4 (KLF4), which suppress NF-κB signaling and drive M2-like polarization, further enhancing immunosuppression [39]. The gene discussed is NFKB1; the disease is glioblastoma.