Furthermore, since Shepherd et al. discovered the elimination of the NTRK2-fusion-harboring cells by Larotrectinib promoted the predominance of untargeted subclone at relapse [95], it is presumed this certain alteration of molecular target might occur much more commonly in recurrence GBM, no matter which treatment we implement, indicating potential obstacles on future glioma therapy. This evidence concerns the gene NTRK2 and glioblastoma.