Furthermore, adding a MET inhibitor overcame the resistance to gefinitib.91 In addition, Akhavan et al. reported that EGFR inhibition promotes PDGFRβ upregulation in glioma cells (Figure 2A-3) and that the combination of EGFR and PDGFRβ inhibitors resulted in more potent antitumor activity in preclinical glioma animal models than either treatment alone.92 As mentioned above, GBM cells treated with EGFR and MET inhibitors may activate NF-κB signaling pathway, resulting in autocrine FGFR activation and SPRY2 overexpression for cellular resistance (Figure 2A-4). This evidence concerns the gene SPRY2 and glioblastoma.