Therefore, to verify the contribution of estrogens and the ER pathway to the response mechanism of breast cancer cells to OA and its derivatives, we performed experiments with MCF7/ER− cells (application of ER inhibitor fulvestrant) and used a cell culture medium devoid of phenol red and charcoal-stripped FBS serum (devoid of growth hormones and cytokines). The gene discussed is GH1; the disease is breast carcinoma.