For instance, Upon stimulation with E2, estrogenic compounds (e.g., genistein, hydroxytamoxifen) or selective GPER agonist G-1, GPER enhanced cancer cell proliferation in the classical-ER-negative breast cancer cells (30) and in the thyroid (95), endometrial (89), and ovarian cancer cells (113), suggesting that GPER may contribute to E2-induced cancer growth. The gene discussed is GPER1; the disease is breast cancer.