GBM has been reported to bear copy number aberrations and overexpression of receptor tyrosine kinases, especially PDGFRA, EGFR (Epidermal Growth Factor Receptor) and MET proto-oncogene, in a significantly non-homogeneous presentation, with subpopulations of the same tumour presenting each genetic alteration in a mutually exclusive, mosaic-like way26,29–32. This evidence concerns the gene MET and neoplasm.