They also found that the efficacy of JQ1 was not compromised by Akt hyperactivation or p53/Rb inactivation, indicated that these often-mutated signaling pathways may not confer resistance to JQ1. The orthotopic GBM tumors also showed significant growth repression with JQ1. The results of these studies support the potential broad therapeutic use of BET bromodomain inhibitors in the treatment of GBM tumors [23]. The gene discussed is DNER; the disease is glioblastoma.