Approximately 70% of breast cancers are ERα+ (ER+), and this receptor remains the primary target for endocrine therapies that aim to block ERα genomic and non-genomic actions with antagonists (tamoxifen, raloxyfen, ICI 182 780), or inhibiting E2 synthesis with aromatase inhibitors [10, 11]. This evidence concerns the gene ESR1 and breast carcinoma.