In the case of glioblastoma (GBM), the most common primary malignant tumor of the central nervous system1, mouse models of GBM-like tumors generated through the genetic disruption of different combinations of core tumor suppressors and/or by introduction of oncogenes such as Src, K-ras, H-ras, PDGFB, and EGFRvIII2 are available to investigate the biology of these aggressive tumors or to test possible treatments in preclinical settings3. This evidence concerns the gene HRAS and glioblastoma.