Therefore, we focused on PLK1 inhibition as the best potential therapeutic lead for TNBC by showing that it is highly expressed in breast cancer cell lines, and its inhibition by PLK1 siRNA as well as BI 2536, an ATP-competitive inhibitor designed to inhibit PLK1 [28], killed the CD44high/CD24-/low population and induced apoptosis. The gene discussed is PLK1; the disease is breast carcinoma.