These multiple complementary preclinical and clinical models, together with quantitative biochemical data, and gene expression and TCGA data analyses, support a model whereby MET cooperates with FGFR to regulate TICs, and where dual inhibition of MET and FGFR1-FRS2 signalling results in TIC depletion, hindering tumour progression in TNBC. Here, FGFR1 is linked to neoplasm.