As primary concern for female health worldwide, the survival outcomes of breast cancer patients differ significantly depending on molecular subtypes.[1, 2] Owing to the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), 15–20% of breast cancers are characterized as triple negative breast cancers (TNBCs), which are the most aggressive subtype with the poorest prognosis.[3, 4] Unravelling the molecular processes responsible for the development of TNBC remains a challenge, particularly to tailor‐made therapy for TNBC patients. This evidence concerns the gene ESR1 and triple-negative breast carcinoma.