MET and neoplasm: Recently, a molecular mechanism was proposed by which ablation of the VEGF/VEGFR-2 signaling cascade increases activity of the hepatocyte growth factor (HGF) receptor MET through a MET/VEGFR-2 heterocomplex and thus promotes tumor cell invasion in glioblastoma [6], although clinical evidence for an effect of MET inhibition in patients with glioblastoma is lacking.