The reliance of ER+ tumours on E has been exploited clinically by the development and use of various endocrine therapies, such as: aromatase inhibitors (AI), which block the conversion of androgens to estrogens; selective ER modulators (SERM), such as tamoxifen, which compete with E for the ER; and fulvestrant (ICI182780), which once bound, potentiates degradation of ER [2]. The gene discussed is ESR1; the disease is neoplasm.