Notably, we previously showed that the signaling mechanism controlling CXCL12-triggered LFA-1 affinity activation is not fully conserved in CLL B-lymphocytes with respect to normal cells [26], with Rac1, CDC42 and PIP5KC possibly bypassed by the neoplastic progression in a group of patients, whereas the role of RhoA is maintained. This evidence concerns the gene CXCL12 and B-cell chronic lymphocytic leukemia.