The epidermal growth factor receptor (EGFR) is over-expressed in various human epithelial tumors usually due to the gene amplification. EGFR gene amplification in tumors frequently contain its rearrangements and among them, the most common extracellular domain mutation is receptor variant III, EGFRvIII (also known as de2-7EGFR or DEGFR). The molecular mass of EGFRvIII is approximately 145 kDa and this genetic change of tumor-specific mutation results from a deletion of 267 amino acids spanning exons 2-7 of the EGFR gene. These consequences make the variant EGFRvIII incapable of binding known ligand. It is expressed in a majority of patients with glioblastoma multiforme. And the evidence shows aberrant EGFRvIII signaling is important for driving tumor progression. MET, also known as c-MET or HGFR (Hepatocyte growth factor receptor), is a transmembrane tyrosine kinase receptor that is encoded in humans by the MET gene. This receptor in charge of tyrosine-kinase activity is mapped at the chromosome 7q31.2 with 1408 amino acids. MET and its ligand HGF/SF (Hepatocyte growth factor/Scatter factor) are expressed in many tissues, principally in epithelial and mesenchymal origin cells, respectively. After binding to ligands, this tyrosine-protein kinase is rapidly internalized, polyubiquitinated and then degraded in a proteasome-dependent manner. MET is over-expressed in numerous types of neoplasms, such as tumors of the kidney, pancreas, thyroid and osteosarcoma. And it is reported that various mutations of MET gene are correlated with papillary renal carcinomas.