This fusion is mutually exclusive with IDH1/2 mutations and EGFR amplification, suggesting its role as an independent driver of GBM progression.130 Additionally, the PTPRZ1-MET fusion represents another oncogenic event, warranting further investigation as a potential therapeutic target.134 The identification of these fusions highlights the importance of personalized treatment strategies in GBM, emphasizing the need for continued research into targeted therapies that exploit these unique molecular alterations. This evidence concerns the gene MET and glioblastoma.