Genetic EGFR alterations (mainly amplifications, but also rearrangements, point mutations and deletions) have been found in about 60% of GBM patients, leading to aberrant EGFR signalling and uncontrolled activation of its downstream pathways (MAPK, PI3K/AKT, JAK/STAT and others), that in turn promote cell and tumour growth, apoptosis resistance and angiogenesis. This evidence concerns the gene EGFR and glioblastoma.