Studies in the 1990s suggested that activated AHR, in at least some cancers, predominantly induced CYP1B1 rather than CYP1A1 transcription [84,93,124,125,126], an outcome that could reflect the contribution of distinct AHR-associated proteins such as the AHR interacting protein (AIP) [127] or differential recruitment of co-activators. The gene discussed is AHR; the disease is cancer.