In GBM, SOX2 contributes to the preservation of self-renewal and enhances the tumor-propagating potential of glioma stem cells (GSCs) via a mechanism involving the indirect inhibition of TET2.36 Consistently, TET2 reconstitution suppresses tumor growth and improves survival in orthotopic GBM models.36 In this context, circulating tumor cells, which share increased tumor-repopulating potential with CSCs, exhibit hypomethylation at several CSC-related genetic loci, including SOX2, POU5F1, and NANOG,37 indicating the existence of strong epigenetic regulation of stemness-related TFs. Here, TET2 is linked to neoplasm.