For example, IDH1 mutations coupled with D-2-hydroxyglutarate accumulation suppress stemness in GBM downstream of inhibited WNT/β-catenin signaling,48 whereas BMP signaling restricts the GSC compartment by favoring the DNMT3A-mediated methylation of PROM1. 49 Moreover, TET1 enhances the expression of NANOG and other pluripotency genes in brain neoplasms by increasing 5-hydroxymethylcytosine (5hmC) marks.50,51 Notably, TET1 has both tumor suppressive52 and oncogenic53,54 effects. The gene discussed is TET1; the disease is neoplasm.