This molecular low-grade group of NF1-associated gliomas was genetically defined by activation of the MAP kinase signaling pathway in isolation without additional oncogenic alterations affecting cell cycle regulatory factors (e.g., CDKN2A, CDK4), telomere maintenance genes (e.g., TERT, ATRX), chromatin modulation (e.g., IDH1/2, histone H3 isoforms, SETD2), or receptor tyrosine kinases (e.g., EGFR, PDGFRA, and FGFR1). This evidence concerns the gene SETD2 and glioma.