Based on multiomic studies, mutations or amplifications in vascular endothelial growth factor—VEGF—(bevacizumab) or EGFR, NTRK fusions (entrectinib or larotrectinib), CDK4/6 gene amplification (palbociclib), and BRAFV600E mutations have been identified as potential therapeutic targets in glioblastoma, among others [4,19]. The gene discussed is EGFR; the disease is glioblastoma.