Interestingly, amplification of the epidermal growth factor tyrosine kinase receptor (EGFR) gene was only seen in 2 patients, well below expected levels for GBM patients and perhaps reflective of the activation of the resultant NTRK fusion protein.6 Our patient was an ideal candidate for targeted therapy in the setting of limited concurrent alterations, a well-characterized activating partner in exon 1 of the BCR gene, and the NTRK2 translocation region.16 This evidence concerns the gene BCR and glioblastoma.