While early studies have demonstrated that FGFR3-TACC3 fusion protein may transform astrocytes into glioma cells in the mouse brain, a recent study showed that tumors harboring FGFR3-TACC3 fusion rely on mitochondrial oxidative phosphorylation for metabolism.26 Furthermore, Day et al. showed that GBM cells can evade EGFR and MET inhibition via FGFR-SPRY2 bypass signaling, and that adding a FGFR inhibitor may increase GBM response to EGFR and MET inhibition.87 Both studies have highlighted the therapeutic potential for treating tumors with FGFR3-TACC3 fusion. This evidence concerns the gene SPRY2 and glioblastoma.