This therapeutic strategy has broad relevance for cancer therapy beyond MB, as the findings are consistent with recent reports where the BET inhibitors (JQ1, OTX015 or RVX2135) and the HDAC inhibitors (panobinostat or vorinostat) synergistically inhibit MYC expression and exhibit antitumor efficacies in preclinical models of neuroblastoma, glioblastoma and lymphoma [26–28]. The gene discussed is MYC; the disease is glioblastoma.