While direct RAS mutations are not very frequent, RAS-related signaling pathways are frequently activated in certain CNS tumors such as GBM, through alternative mechanisms like EGFR amplification, NF1 loss, and PDGFR overexpression, which converge on the RAS/RAF/MEK/ERK and PI3K/AKT axes. This evidence concerns the gene NF1 and glioblastoma.