The observed interaction of c-Met with many of the tumorigenic pathways discussed in this review that drive treatment resistance, EMT and CSC maintenance, angiogenesis, proliferation, and invasion/metastasis in various tumors implicates c-Met as being one of the key players in cancer malignancy and that multi-modality targeted therapy aimed at inhibiting these redundant and compensatory pathways may show promise in therapeutic efficacy. Here, MET is linked to cancer.