Overexpression and mutations in EGFR lead to a more aggressive glioblastoma phenotype and increased tumor heterogeneity, therefore several strategies have been developed to target EGFR (Table 2) (87, 89, 161, 162) B7-H3 (also known as CD276) is a type I transmembrane protein, that expressed in >70% of glioblastoma patients (163, 164), and is associated with progression, metastasis, poor outcome and immune evasion (165), as it is an immune checkpoint molecule expressed on antigen-presenting cells. The gene discussed is EGFR; the disease is neoplasm.