Inhibition of NF-κB pathway or antiapoptotic proteins overcomes IBR+VEN drug resistance in CLL and MCL cells preincubated with agonist mix. (A-F) The NF-κB pathway inhibitor BMS-345541 (A) and Bortez (B) and antiapoptotic protein inhibitor UMI-77 (Mcl-1 inhibitor) (D), BH3I-1 (Bcl-xL inhibitor) (E), and YM155 (survivin) (F) were tested in increasing concentrations with or without IBR (0.1 μM) + VEN (25 nM) in CLL (Pts 01, 03, and 12) and a MCL (Pt 45) patient PBMC preincubated with agonist mix as shown in Figure 2A. The antiapoptotic protein inhibitor A1210477 (C) was similarly tested in 4 CLL patient samples (Pts 03, 33, 35, and 46). Cell viability was determined using an alamarBlue assay. The data were normalized to DMSO treatment control or IBR+VEN in triple drug treatment. The data presented as means ± SD. ↓ indicates drug concentration at which target kinase phosphorylation/signaling pathway/apoptotic protein was maximally inhibited, based on published values.^56-59