AHR and neoplasm: Paradoxically, acute activation of the AhR by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) inhibits tumor cell proliferation through mechanisms that involve upregulation of the CDK inhibitor p27Kip1, binding of the pRB tumor suppressor, suppression of E2F-mediated transcription as well as inhibition of hormone signaling [9-11].