In contrast, primary GBM, which are nearly all IDH Wild-type, are typically displaying epidermal growth factor receptor (EGFR) and mouse double minute 2 homolog (MDM2) amplification or mutation, cyclin-dependent kinase inhibitor 2 A/B (CDKN2A/B) deletion, phosphatase, and tensin homolog (PTEN) loss and neurofibromatosis type 1(NF1), and telomerase reverse transcriptase (TERT) promoter mutations, along with the gain of chromosome 7 and loss of heterozygosity at q10 (LOH 10q) (chromosome 10) (25). This evidence concerns the gene IDH1 and glioblastoma.