In fact, inhibition of TAK1 in mantle cell lymphoma had a more pronounced effect on cellular proliferation than the NF-κB inhibitor used as a positive control, more than likely due to the fact that TAK1 impacts the activity of other survival regulators in addition to NF-κB, including p38 and XIAP.32 These data suggest that while NF-κB appears to be the ultimate driver of abnormal B-cell activity in MYD88L265P-expressing cells, targeting MYD88 signaling further upstream of NF-κB may be more effective clinically. This evidence concerns the gene XIAP and mantle cell lymphoma.