This hypothesis can be extended to the different clinical breast cancer subtypes, which are defined based on expression of hormone receptors and human epidermal growth factor receptor 2 (HER2) and on identification of transcriptional signatures (4), referring to luminal breast cancer [roughly equivalent to tumors expressing estrogen receptor (ER) and/or progesterone receptor (PR)], HER2+, and triple-negative breast cancer (TNBC), lacking expression of ER, PR, and HER2. This evidence concerns the gene ESR1 and triple-negative breast carcinoma.