Dysregulated activation of indoleamine 2,3-dioxygenase (IDO1) and tryptophan 2,3-dioxygenase (TDO) in tryptophan metabolism significantly alters the tumor microenvironment (TME), and simultaneous accumulation of kynurenine (Kyn) activates the aryl hydrocarbon receptor (AhR), promoting the production of FoxP3+ regulatory T cells, which eventually leads to immune escape (4). The gene discussed is AHR; the disease is neoplasm.