Endocrine therapy drugs either reduce E2 availability (e.g., aromatase inhibitors (AIs)) or block ERα activity by directly binding to the receptor; 4OH-tamoxifen (4OH-Tam), a selective ER modulator (SERM), inactivates ERα transcriptional activity, and fulvestrant (ICI182,780-ICI), a selective ER downregulator (SERD), eliminates ERα from BC cells and prevents receptor transcriptional functions [1]. This evidence concerns the gene ESR1 and breast cancer.