They demonstrate that estrogen, as well as SERMs and SERDs, such as tamoxifen, fulvestrant and raloxifene, continues to activate multiple signaling pathways in the absence of ER through the G protein-coupled estrogen receptor GPR30/GPER and that estrogen-stimulated ER-negative endometrial tumor growth is blocked by a selective GPER antagonist. The gene discussed is GPER1; the disease is endometrium neoplasm.