Thus, these studies have lent credence to the argument that: (1) primary cancer prevention can be effected by minimizing exposure to subsets of environmental AHR ligands, (2) cancer interception can be considered prior to full blown malignancy if early markers of AHR activity can be identified (e.g., Figure 3), and (3) several cancers in which AHR levels correlate with poor survival may be treatable with specific AHR inhibitors. The gene discussed is AHR; the disease is cancer.