Mouse models characterized by conditional and tissue/cell-specific expression of multiple genes simultaneously or developed by altering key signaling pathways involved in GBM (such as Egfr, Nf1, Ras, Pten) are recently used, improving the genetic and phenotypic heterogeneity of mouse gliomas, that are typical of human GBM. The gene discussed is NF1; the disease is glioblastoma.