In models of acute lymphoblastic leukemia and glioblastoma, BETI induced cell death independently of p53 signaling.15 However, in acute myeloid leukemia cells harboring mutations in DMNT3A, BETI combination with known activators of p53, induced cell death via a p53 mediated pathway.16 Using Eμ-myc lymphomas, deficient for p53 or its activator p19Arf, we show that a functional p53 pathway was not necessary for the apoptosis-inducing effects of I-BET762. The gene discussed is TP53; the disease is glioblastoma.