Like other BH3 mimetics, quantitative expression levels of BCL-2 proteins alone were not effective indicators of sensitivity to BIM SAHBA. However, given the natural affinity of the BIM BH3 death domain to engage all anti- and pro-apoptotic BCL-2 proteins, it was not surprising that the cell permeable hydrocarbon-stapled BIM BH3 therapeutic reactivated cell death in all DLBCL tested. This evidence concerns the gene BCL2L11 and diffuse large B-cell lymphoma.