In a very elegant work, Niola and colleagues combined LV-mediated overexpression of oncogenic H-Ras, silencing of the oncosuppressor p53 and Cre-loxP technology to generate a mouse model of high-grade GBM and to study the role of Inhibitor of Differentiation (ID) proteins in TIC biology and tumor maintenance [102]. The gene discussed is HRAS; the disease is glioblastoma.