Here we report genetic studies designed to clarify whether BH3-only proteins act as tumor suppressors during AML development and which of them are critical for the response of MLL fusion gene-driven AMLs to standard chemotherapeutics (cytarabine, daunorubicin and etoposide) or to the proteasome inhibitor bortezomib, which is being trialed clinically for AML.42, 43 We also tested whether the MLL AMLs are sensitive to ABT-737, and whether combination therapy with ABT-737 improves sensitivity. The gene discussed is KMT2A; the disease is neoplasm.