These include MET gene amplification (mainly observed in stomach and lung cancer), causing overexpression and ligand‐independent activation of MET [15, 16, 17, 18, 19, 20], alterations (mostly observed in glioblastoma) causing HGF overexpression leading to aberrant MET activation through establishment of an autocrine loop [21, 22], and chromosomal rearrangements leading to MET fusion with another gene (observed in lung adenocarcinoma and renal cell carcinoma), inducing either constitutive activation or overexpression of MET [23]. Here, MET is linked to glioblastoma.