Current therapies for ER+ breast cancer rely heavily on their ability to block ER signaling either by inhibiting the synthesis of estradiol (aromatase inhibitors (AIs)) or by inhibiting ER signaling through competitive binding to the receptor itself [selective estrogen receptor modulators (SERMs) and selective estrogen receptor degraders (SERDs)] [6–9]. The gene discussed is CYP19A1; the disease is breast carcinoma.