BCL-2 family members appear to repress apoptosis in part by inhibiting the effects of proapoptotic BH3-only proteins, such as BIM or BCL-2-associated death promoter.18 Based on our observation that v-Abl-transgenic tumor cells expressing the miR-shRNA targeting A1 were found more sensitive to imatinib, we conclude that v-Abl-kinase signaling promotes survival at least in part by increasing the ratio between A1 and BIM expression levels. Here, BCL2L11 is linked to neoplasm.