The abundance of signal transducer and activator of transcription 3 (STAT3) in GBM has been demonstrated to promote AHR expression and cooperate with HIF-1α to increase CD40 levels, which in turn promoted GBM immune evasion and STAT4-mediated PD-L1 upregulation (42, 51, 55). This evidence concerns the gene HIF1A and glioblastoma.