ER+ and/or PR+ tumors represent more than two-thirds of breast cancer cases and are currently treated with hormonal therapies that most commonly include aromatase inhibitors, which suppress endogenous estrogen production, or antiestrogens, which compete with estrogens for binding to estrogen receptors and inactivate them by inducing alternative conformations of their ligand-binding domains [4,5]. The gene discussed is ESR1; the disease is breast carcinoma.