Recent genomic profiling studies have indeed shown overactivation of receptor tyrosine kinase pathways via tyrosine phosphorylation as the most commonly altered phenomena in glioma, with more than 80% of glioma displaying epidermal growth factor receptor (EGFR) constitutive TP and subsequent tyrosine kinase burst [5], [6]. The gene discussed is NTRK1; the disease is central nervous system cancer.