In addition to promoting chemoresistance, the ability of CLL cells to access and be retained within the bone marrow (BM) and lymph node (LN) microenvironment increases their chance of encountering proliferative signals such as antigenic stimulation of the B cell antigen receptor (BCR), or the T cell factors CD154 (CD40 ligand) and interleukin 4 (IL-4) [5], ultimately resulting in disease progression. This evidence concerns the gene BCR and B-cell chronic lymphocytic leukemia.