Cells were treated with imatinib (Gleevec, Selleckchem, Munich, Germany), a clinically used BCR-ABL inhibitor that induces apoptosis depending on the BH3-only protein and established A1 antagonist, BCL-2 interacting mediator of cell death (BIM).18 In addition, we tested the response of these tumor cells to the BH3-mimetic ABT-737 that inhibits BCL-2, BCL-X and BCL-W but not MCL-1 or A1.19 Compared with immortalized WT controls, cells derived from VV-A1 knockdown mice were found more responsive to imatinib or imatinib plus ABT-737 (Figure 1e). The gene discussed is BCL2L11; the disease is neoplasm.