This discrepancy implies the presence of distinct NF-κB complexes in different CLL cases, and, coupled with our observation that RelB and p52 are rapidly and continuously activated during CD40L-stimulated proliferation, suggests that as well as canonical signalling, non-canonical NF-κB signalling contributes to CLL cell survival and proliferation. This evidence concerns the gene RELB and B-cell chronic lymphocytic leukemia.