The MET gene (a.k.a. c-Met) is located in the chromosomal region 7q31.2 and encodes a transmembrane tyrosine kinase receptor for the hepathocyte growth factor (HGF). HGF and MET play an important role in angiogenesis and tumor growth. Activation or upregulation of MET was found in a number of carcinomas including lung, breast, colorectal, prostate, and gastric carcinomas as well as in gliomas, melanomas and some sarcomas. MET overexpression is known as a negative prognostic indicator in patients with various carcinomas, multiple myeloma, or glioma. Therefore, several inhibitors of the HGF/MET signaling pathway are being studied and developed as potent therapies to inhibit angiogenesis and tumor growth. Recently, it was shown that MET amplification leads to resistance to gefitinib or erlotinib in lung cancer by driving ERBB3-dependent activation of the PI3K pathway.