AHR and glioblastoma: Endogenous Trp derivatives, such as Kyn and ITE (2-(10H-indole-30- carbonyl)-thiazole-4-carboxylic acid methyl ester), may play opposite roles in cancer progression and stemness, regulating OCT4 expression through AhR modulation: accumulation of the low-affinity AhR agonist Kyn in the tumor microenvironment favor carcinogenesis, whereas the high-affinity AhR agonist ITE promotes its binding to the OCT4 promoter to suppress its transcription and, consequently, inducing cell differentiation in U87 glioblastoma neurospheres [49].