Triple‐negative breast cancer (TNBC), characterized by the absence of the oestrogen receptor (ER), the progesterone receptor (PR), and the human epidermal growth factor receptor 2 (HER2) expression, was known as the most aggressive breast cancer subtype.1 TNBC patients have a higher risk of distant metastasis and a poorer overall survival than other breast cancer patients, partly due to lacking effective targeted therapies.2 Despite the great effort made on researching TNBC, the molecular mechanisms underlying TNBC aggressive behaviour are still obstacles to TNBC treatment. The gene discussed is PGR; the disease is breast carcinoma.