FGFR fusions are the most common, present in 8.33% of cases, followed by EGFR (4%) and ALK (1.9%), with the latter being more prevalent in pediatric GBM.130 NTRK1 fusions, although rare (1.2%), may contribute to GBM oncogenesis.131 Clinically, inhibitors such as lorlatinib and larotrectinib show promise in targeting fusion-positive GBMs.132,133 FGFR3-TACC3, a recurrent fusion protein, drives tumorigenesis by promoting kinase transphosphorylation and disrupting chromosomal stability. This evidence concerns the gene TACC3 and glioblastoma.