While overexpression of hepatocyte growth factor (HGF) by stromal or tumor cells may result in ligand-dependent MET activation in a paracrine or autocrine manner [4, 5], focal amplification of the MET receptor gene (METamp) [6, 7], its point mutation (METmut) [8, 9], or alternative splicing of its mRNA [10, 11] also may cause a ligand-independent MET activation. This evidence concerns the gene MET and neoplasm.