TP53 and glioblastoma: To determine whether a lower ATIP1 expression is dependent on this hypermethylation, we subsequently treated the cells with decitabine (5-Aza-dC), a hypomethylating agent, which resulted in the re-expression of ATIP1 at the transcriptional and translational level in all GBM and GSC cells tested so far, irrespective of the p53 status of these cells (Figure 2c–e), suggesting that hypermethylation is partially responsible for MTUS1/ATIP1 downregulation in HGG.