Taken together, our data support that MET and FGFR1-FRS2 pathways cooperate to promote a population of mesenchymal-like TICs in TNBCs and, consistent with other potential therapies targeting mesenchymal-like TIC populations90,91, the clinical benefits of inhibiting these receptors are likely maximised if paired with tumour de-bulking by a chemotherapeutic agent. The gene discussed is MET; the disease is neoplasm.