MET and glioblastoma: Many of them result in aberrations of signaling molecules and pathways potentially regulated by APPL proteins, like RTKs (mutational activation or amplification of EGFR, PDGFRA and HGF receptor MET) and AKT (inactivating mutations and deletion of PTEN, activating mutations of genes encoding PI3K complex PIK3CA and PIK3R1, amplification of AKT3), highlighting their importance for GBM development and further supporting the choice of glioma as our experimental model.