Specifically, HDAC1 is not only upregulated by NANOG151 but also reinforces the tumorigenic potential of GSCs by repressing p53-mediated tumor suppression.152 HDAC2 enhances stemness and GSC-driven tumorigenesis in conjunction with transforming growth factor beta (TGF-β) signal transducers such as SMAD family member 3 (SMAD3) and SKI proto-oncogene (SKI), at least in part by upregulating genes such as SOX2 and OLIG2. 153 Moreover, HDAC3 fosters GSC-related gliomagenesis by engaging GLI1 signaling,154 whereas HDAC6 supports GSC maintenance by modulating Hedgehog signaling.155. This evidence concerns the gene SMAD3 and neoplasm.