Of note, over-activation of the HGF/MET pathway through germline MET and sporadic MET mutations or even protein over-expression increases tumorigenesis and tumor progressions in numerous cancer forms, such as renal cell carcinoma, metaplasia-dysplasia-adenocarcinoma evolution in esophageal cancer, osteosarcomas, and melanomas, as well as brain, gastric, gliomas, breast, and head and neck cancers [1, 4–6]. This evidence concerns the gene MET and renal cell carcinoma.