EGFR and glioblastoma: Presently, omics profiling identifies three GBM subtypes: proneural, classic, and mesenchymal [27], each characterized by different genetic alterations and molecular signatures, as epidermal growth factor receptor (EGFR) gene amplification or mutation, telomerase reverse transcriptase (TERT) promoter mutation, homozygous loss of cyclin-dependent kinase inhibitor 2 A/2B (CDKN2A/2B) gene, phosphatase and tensin homolog (PTEN) gene deletion or mutation, gain of chromosome 7, and loss of the entire chromosome 10 [27, 28].