Aromatase inhibitors (AIs) are the standard of care as first-line treatment for postmenopausal women with oestrogen receptor positive (ER + ) advanced breast cancer (BC).1 However, the objective response rate to AIs in the metastatic setting is between 20%–40% and virtually all patients eventually relapse with AI-resistant disease.2,3 It is critical to understand the molecular drivers of the resistance to allow rational use of subsequent or concurrent therapy. This evidence concerns the gene ESR1 and breast carcinoma.