In most cases, GBM arises as primary tumors, comprising a plethora of genetic and epigenetic alterations which frequently include the overamplification and activating of mutations in the epidermal growth factor receptor (EGFR), inactivating mutations and/or deletions in the tumor suppressor phosphatase and tensin homolog (PTEN) and the cyclin-dependent kinase inhibitor A (CDKN2A) genes; all these changes lead to the overactivation of core signaling pathways such as RAS/RAF/MAPK, PI3K/AKT, or cyclin-dependent kinases 4 and 6 (CDK4/6) [7]. Here, EGFR is linked to glioblastoma.