The demonstration that both malignant cells and stromal or fibroblast-like cells within the tumor microenvironment (TME) express high AHR levels, as first shown in 2000 [85] and later confirmed [100], suggested that the influence of the AHR in cancer may not be limited to acute induction of mutagenic intermediates and that the contribution of the AHR to cancer progression in the TME, as with most things AHR, may be complex and ongoing. The gene discussed is AHR; the disease is cancer.