The increased activity of AHR in mesenchymal glioblastoma is of particular interest, as this subtype does not differ in AHR expression from the other glioblastoma subtypes 89, suggesting that it is not the abundance of the transcription factor, but that of its potentially Trp-derived agonists that leads to the increase in AHR activity in mesenchymal glioblastoma. Here, AHR is linked to glioblastoma.