Kolasa and colleagues found, in a human breast cancer cell (MCF-7) line, that simultaneous exposure to environmental PAHs and tumor necrosis factor (TNF)-α induced increased expression of IL-6 and that this effect could be counteracted by silencing the AhR, implying that AhR may have a key role in IL-6 regulation within the tumor microenvironment (93). This evidence concerns the gene IL6 and neoplasm.