While this driver mutation is highly conservative and unique, much attention has been paid to its histone biology, and more specifically in relation to H3.3 mutations in glioblastoma et vice versa. Here, we focus on the possible relations between the G34W mutant stromal cell and other cell biological features which are characteristic for GCTB, such as the presence of TAs, its slight cytogenetical instability, the reactivation of hTERT, and its loss of control of RANKL secretion (see Figure 3). This evidence concerns the gene TNFSF11 and glioblastoma.