Supporting evidence for this theory includes 1) the association of IDH1 mutations with glioma evolution, glioma CpG island methylator phenotype, and proneural subtype; 2) the induction of methylator phenotype in normal human astrocyte by IDH1R132H transduction or D2-HG treatment; and 3) the association of IDH1 mutations with repressive histone methylation marks that contribute to a less differentiated or stem-like state [5]. The gene discussed is IDH1; the disease is central nervous system cancer.