MET receptor tyrosine kinase (RTK) is a proto-oncogene that is frequently aberrantly activated in cancer through gene amplification and/or activating mutations that result in hypersensitivity to HGF stimulation or HGF-independent activation. Oncogenic MET activation can occur as a primary mechanism of malignant transformation or be selected secondarily, as a mechanism of resistance to therapeutics that target related RTKs, such as EGFR. MET targeted anti-cancer therapeutics, either recombinant monoclonal antibodies (MAbs) or small tyrosine kinase inhibitors (TKIs), have shown promise as a first-line agents for the treatment of solid tumors with primary MET activation or as second-line agents for the treatment of solid tumors with acquired MET-mediated resistance to other RTK-targeted therapies (reviewed in Comoglio et al. 2018).