Primary GBMs are typically wild type (WT) for isocitrate dehydrogenase 1/2 (IDH), with no IDH-mutant associated hypermethylated phenotype (termed glioma CpG island methylated phenotype (G-CIMP)), while secondary (progressive) GBMs often arise from IDH-mutant lower-grade gliomas1,3–7. This evidence concerns the gene IDH1 and glioma.