EGFR and neoplasm: For example, we do not believe that an IDH-wildtype glioblastoma aligning with the RTK2 methylation class of adult glioblastomas that has TERT promoter mutation, CDKN2A/B homozygous deletion, EGFR amplification, and combined trisomy 7 plus monosomy 10 with low tumor mutation burden at time of initial resection which acquires hypermutation and mismatch repair deficiency at time of recurrence/progression should be considered equivalent to the de novo RRD glioblastomas described in this study.