Indeed, it has been demonstrated that the anti-proliferative effects of PPARγ in MCF-7 breast cancer cells are mediated, at least in part, by the opposite interplay exerted by ERα and PPARγ pathways on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling, whose activation induces breast cancer cell proliferation. This evidence concerns the gene ESR1 and breast carcinoma.