EGFR and glioblastoma: As above mentioned, the majority of glioblastomas harbor an amplification and or mutation of a RTK, either EGFR (occurring in 40 to 50% of cases) or PDGFRA (occurring in approximately 15% of cases) Given these findings, EGFR and PDGFRA have been regarded as primary candidates for therapeutic targeting: however, initial clinical trials with small-molecule inhibitors targeting these receptors have shown very limited responses and this seems to be due to a great intratumoral heterogeneity of RTK abnormalities.