MET and glioblastoma: The c-Met/HGFR receptor tyrosine kinase is a promising therapeutic target as mutations of c-Met (in papillary renal cell carcinoma, childhood hepatocellular carcinoma) and focal amplifications of the MET gene locus (in NSCLC, GBM, esophageal and gastric cancers) may indicate an oncogenic dependence on c-Met signaling [6], [7], [8].