GBM displays remarkable intratumoural heterogenicity, bearing multiple genetic or epigenetic alterations5, such as loss of PTEN and P53; amplification of receptor tyrosine kinases (RTKs); inactivation of CDKN2A (p16/INK4A) and CDKN2B; and mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2, a discriminant between primary and secondary GBM6,7). This evidence concerns the gene NTRK1 and glioblastoma.