Compared with a propensity score–matched NF1 wild-type, IDH wild-type glioblastoma cohort (Supplemental Table 2), NF1-mutant glioblastomas were significantly more likely to harbor comutation of PTPN11, an upstream Ras regulator, while NF1 wild-type glioblastomas were significantly more likely to harbor EGFR amplification and amplification of cell cycle/apoptosis–associated oncogenes CDK4, MDM2, or MDM4 (Figure 1B). The gene discussed is EGFR; the disease is glioblastoma.