EGFR amplification occurred in 44% of our cohort, which is consistent with previous genomic analyses reporting that approximately 50% of GBMs harbored EGFR alterations.6  EGFR is a receptor tyrosine kinase that induces downstream signaling through RTK/PI3K pathways, among others, to induce cellular differentiation and proliferation and play a causal role in tumorigenesis.40 Though hypothesized to serve as a potential prognostic biomarker for GBM, there lacks a consensus regarding the impact of EGFR amplification on clinical outcomes. Here, NTRK1 is linked to glioblastoma.