TP53 and glioblastoma: 38 Further analysis of the cluster associated with high ID2 revealed that this cluster includes tumors belonging to each of the different molecular subtypes of GBM (Supplementary Figure 5a),39, 40 and that loss-of-function alterations in TP53 were common in this group (39% of patients), which we have previously shown as a mechanism that can drive ID2 transcription.41 There were, however, no overall survival differences between patients represented in this cluster and we identified no clinical parameters that distinguished patients within this cluster(Supplementary Figure 5b).