Consistent with the notion that the membrane-proximal ITAM tyrosine of CD79b might drive BCR internalization, mutation of CD79b Y195 to either glutamic acid (E, a mutation very similar to the tyrosine to aspartic acid [D] mutation found in multiple ABC DLBCLs) or to alanine (A, a more conservative substitution) completely blocks CD79-driven internalization. This evidence concerns the gene BCR and aneurysmal bone cyst.