Genomic analysis of a small group of GBM patient samples suggests that the TET2 loci is prone to hypermethylation leading to repression, providing an alternative explanation for the robust loss of 5hmC observed in GBM.34 We now show, for the first time, that forced expression of reprogramming transcription factor SOX2, which is highly expressed in GBM, reduces expression of TET2 and 5hmC (Fig. 1f, g), thus contributing to the hyper-methylated phenotype of GSCs (Fig. 1h). The gene discussed is TET2; the disease is glioblastoma.