To test whether such mechanisms could explain the relatively low expression of PREX1 in PriGO17A cells, these cells were treated with the HDAC inhibitor Trichostatin A. This led to an increase in PREX1 levels in PriGO17A (Figure 1C), supporting a role for histone modifications in controlling PREX1 expression in glioblastoma. Here, HDAC9 is linked to glioblastoma.