The overexpression of prosurvival proteins, such as Bcl-2 or Bcl-6, through translocation or amplification, leads to mitochondrial damage protection and often correlates with drug resistance and poorer prognosis in patients with B-cell lymphoma.1 To determine the importance of mitochondrial damage in BETI-mediated apoptosis, we took advantage of Eμ-myc/bcl-2 lymphomas and human B-cell lymphoma cell lines refractory to standard care of therapy (U2932-4RH, Raji-4RH and RL-4RH), and investigated their sensitivity to I-BET762 in vitro. The gene discussed is BCL2; the disease is lymphoma.