Our analyses provided unequivocal evidence that RelB:p50 dimer not only cooperates with RelA:p50 but transcription-activating function of RelB:p50 circumvents the requirement of RelA in mediating pro-survival TNF response in p100-depleted cells, including myeloma cells harboring non-canonical mutations (Figures 5, 6, 7). This evidence concerns the gene RELB and plasma cell myeloma.