The molecular landscape of adult-type diffuse gliomas is characterized by mutation involving the TERT promoter leading to telomerase activation or an alternative lengthening of telomere phenotype (ALT), most commonly attributed to ATRX mutation, and less commonly due to H3 mutation.9,10 While H3G34R/V is a common mutation implicated in hemispheric gliomas in the spectrum of H3-mutant gliomas,11 the positivity for OLIG2 and lack of p53 overexpression seen in our case make it less likely to be H3G34-mutant. This evidence concerns the gene GPT and central nervous system cancer.