Extensive molecular characterization of glioblastoma multiforme (GBM) achieved through The Cancer Genome Atlas (TCGA)1–3 has revealed a number of genes that are significantly mutated, namely PTEN, TP53, EGFR, PIK3CA, PIK3R1, NF1, RB1, and PDGFRA, where EGFR and PDGFRA gene amplifications are among the most common genetic aberrations of receptor tyrosine kinases in GBM occurring in 57.4% and 13.1% of patients, respectively1. The gene discussed is NF1; the disease is glioblastoma.