The lack of estrogen receptor α (ERα) expression in most type II tumors has led to the assumption that these tumors must be “estrogen-independent” and that treatment with antiestrogens (selective estrogen receptor modulators (SERMs) such as tamoxifen and Raloxifene, or pure antagonists/selective estrogen receptor modulators (SERDs) such as ICI182,780/fulvestrant) commonly used in breast cancer treatment, would be ineffectual, a conclusion largely substantiated in a number of clinical trials [5, 6]. Here, ESR1 is linked to breast cancer.