FOXG1 and glioblastoma: They found that EGFRvIII, the most common EGFR mutation, sensitizes GBM cells to the BET-bromodomain inhibitor JQ1 in this SOX9, FOXG1-dependent manner, thereby identifying the role of epigenetic and transcriptional remodeling in EGFR-dependent tumorigenesis and suggesting a plausible basis for epigenetic therapy [38].