Access to the FDCs, which is controlled by the CXCL13–CXCR5 chemokine signaling axis, confers proliferative stimuli upon the leukemia B cells, as demonstrated in the immunoglobulin heavy chain (IgH) enhancer T-cell leukemia-1 oncogene (Eμ-Tcl1) transgenic mouse model of CLL [14]. This evidence concerns the gene CXCR5 and B-cell chronic lymphocytic leukemia.