CXCR4 and B-cell chronic lymphocytic leukemia: Complement-dependent cytotoxicity is the mechanism in focus in this study since complement has been reported as essential to the therapeutic activity of rituximab in murine lymphoma models [27, 28] and since disruption of CLL-stromal cell interaction by CXCR4 antagonism in vitro was demonstrated to increase the efficacy of rituximab-induced complement-dependent cytotoxicity, whereas this was not the case for rituximab-induced antibody-dependent cellular cytotoxicity [21].