The development and maintenance of MYC-driven B-cell lymphoma in laboratory mice requires suppression of MYC-dependent apoptosis by MNT. The new findings firmly establish MNT as an oncogenic collaborator of MYC in neoplastic B-cell development. The underlying mechanism relies on MYC-dependent downregulation of BIM¹⁰  (eg, BCL-2 like 11 [BCL2L11], a member of the apoptosis-initiating family of BH3-only proteins that also includes BID [BH3 interacting domain death agonist], and PUMA [BCL2 binding component 3 or BBC3]). BIM is a negative regulator of survival-enhancing BCL2 (BCL2 apoptosis regulator) family proteins that also include MCL1 (MCL1 apoptosis regulator) and BCL-X_L (eg, BCL2 like 1, BCL2L1) and prevent activation of pro-apoptotic effectors BAX (BCL2-associated X) and BAK (eg, BCL2 antagonist/killer 1 or BAK1). Low BIM expression in the presence of MNT (indicated by thin arrow at the top left) results in upregulation of BCL2 proteins supporting B-cell survival by keeping BAX and BAK in an inactive state. Enhanced survival sets the stage for malignant growth driven by MYC because it buys tumor precursors time to pick up the secondary (epi)genetic changes required for full malignant cell transformation (vertical pathway on the left). In the absence of MNT, because of genetic knockout targeted to B lymphocytes, MYC-dependent activation of BIM is unrestrained (depicted by thick arrow, top right), which leads to high levels of BIM, strong suppression of BCL2 proteins and execution of programmed cell death via activation of BAX and BAK. In this circumstance, the pool of tumor precursors containing active MYC is unable to expand and lymphoma development is essentially abrogated (vertical pathway on the right).