In these scenarios CCL19 and CCL21 can act as single factors that activate mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K)-AKT signaling (40, 70) or in a cooperative fashion with CXCL13 which contributes to resistance of CLL cells (but not normal CD5+ B-cells) to TNF-α-mediated apoptosis through up-regulation of PEG10 which in turn stabilizes caspases-3 and -8 (26, 27). This evidence concerns the gene CCL21 and B-cell chronic lymphocytic leukemia.