Combined with the notion that AhR-mediated transcriptional induction of CYP1A1 is essential for the cytotoxicity of AF, these data not only indicate crosstalk between ERα and AhR pathways in the response of breast cancer cells to AF, but also raise the possibility that reactivation of ERα in mesenchymal-like TNBC cells could restore AhR responsiveness and thus sensitize these cells to AF. The gene discussed is AHR; the disease is breast cancer.