As a result, we could consider that CXCL13 and galectin-9 cooperate preferentially to provide a suitable tumor microenvironment by supporting the CLL cell survival, growth, proliferation, and invasion and enhancing antiapoptotic activity through CXCL13/CXCR5, galectin-9/Tim-3 pathways as well as several immunosuppressive mechanisms like enhancing the function myeloid-derived suppressor cells and exhaustion of T cell [12, 17]. The gene discussed is CXCR5; the disease is neoplasm.