On the other hand, the clinical and molecular characteristics of adult H3K27M-mutant DMGs also differ from IDH-wildtype glioblastomas, the former having an earlier age of diagnosis, exclusive midline location, and less frequent methylation of MGMT promoter and no EGFR amplification.3,4 Recent studies have also identified CDKN2A/B homozygous deletions as a frequent event and an independent poor prognostic factor in IDH-wildtype glioblastoma.14 The lack of homozygous CDKN2A/B deletions could have, in part, contributed to the prolonged survival of our patient. Here, EGFR is linked to glioblastoma.