Since 2H-DNA-bearing cells can be identified by the reciprocal surface densities of CXCR4 and CD5 [2], a 3-subpopulation model was developed which proposed that when CLL cells divide in tissue proliferation centers, they upregulate surface membrane (sm) CD5 levels and reduce smCXCR4 and various integrin/cell adhesion molecules [1,2]. This evidence concerns the gene CXCR4 and B-cell chronic lymphocytic leukemia.