Complex mechanisms are proposed to explain the anti-estrogenic nature of AhR in breast and other cancers [132, 133] that are associated with the direct interaction with ER, resulting in the inhibition of DNA binding and disruption of coactivator/repressor recruitment [134, 135], that are associated with the anti-proliferative and pro-apoptotic effects of AhR agonist [136]. Here, ESR1 is linked to cancer.