For CCR7-dependent B-ALL, CNS entry was linked to ZAP70 activation, as described previously [256], whereas, for primary central nervous system lymphoma, astrocyte-derived CCL19 retained CCR7-expressing lymphoma cells in the CNS, leading to gliosis and increased risk of gliosis-induced primary central nervous system lymphoma [292]. The gene discussed is ZAP70; the disease is precursor B-cell acute lymphoblastic leukemia.