IDH-mutant gliomas can be further differentiated by the ATRX, CDKN2A/B, and TP53 status, whereas the TERT mutation, EGFR amplification status, MGMT promotor methylation status, and whole gain of chromosome 7 and whole loss of chromosome 10 status can further differentiate IDH-wildtype GBM [2,3,4]. This evidence concerns the gene IDH1 and central nervous system cancer.