We also show here that cases with unmutated IGHV had a higher level of RelB DNA binding activity than cases with mutated IGHV (Figure 2) and hypothesise that RelB function may be important in this CLL subtype, which is known to have more proficient signalling via the BCR and is reliant on pro-survival signals from the microenvironment [25]. The gene discussed is BCR; the disease is B-cell chronic lymphocytic leukemia.