Because genetic alterations in RTKs, such as FGFRs, EGFR, HER2, MET, ALK, and RET, drive human cancers, small-molecule inhibitors and human/humanized monoclonal antibodies targeted against RTKs have been developed as cancer therapeutics (Ciardiello and Tortora, 2008; Kwak et al., 2010; Mologni, 2011; Buettner et al., 2013; Katoh and Nakagama, 2013; Li et al., 2013). This evidence concerns the gene MET and cancer.