While genetic alteration of RAS is rare in adult human GBM (accounting for ~1% of cases; refs. 69, 70), RAS can be activated as a downstream target of amplifications/mutations in EGFR (amplified or mutated in 45% and 26% of GBM patients, respectively), PDGFRA (13%), ERBB2 (8%), and MET (4%), or deletion or mutation of its negative regulator NF1, which is found in about 10% of GBM patients (6). Here, EGFR is linked to glioblastoma.