Kyn activates the aryl hydrocarbon receptor (AhR) in T cells, leading to T cell anergy, impaired cytotoxicity, and the induction of Treg differentiation.[113] Unlike effector T cells, Tregs exhibit greater metabolic adaptability and can maintain their suppressive function in nutrient‐deprived environments by relying more heavily on oxidative phosphorylation and utilizing alternative substrates such as fatty acids or tumor‐derived lactate.[114] Moreover, AhR signaling in Tregs enhances FoxP3 stability and reinforces their immunosuppressive phenotype. This evidence concerns the gene AHR and neoplasm.