The heterogeneity of GB tumors, in which EGFR deletion and EGFR amplificated mutations can coexist in different cells, leads to adverse effects arising from collateral inhibition of EGFR in normal tissues, as well as to redundant and alternative compensatory pathways, which represent the most important escape mechanisms that limit the anti-glioma effects of the different EGFR-targeting drugs [536,537,538,539]. Here, EGFR is linked to glioma.