To test whether the differences in the apparent dimer formation between the tonic BCRs from primary and Burkitt lymphoma B cells and the CLL-derived BCR are indeed caused by autonomous self-aggregation of the latter, we replaced an arginine residue within the CLL VH domain, which lies within a motif that was reported23 to serve as ‘auto-antigen’ for chronic activation of CLL-derived BCRs, with alanine (R38A) and analyzed this mutant CLL-BCR as before. This evidence concerns the gene BCR and B-cell chronic lymphocytic leukemia.