This can be accomplished by a transpresentation of the chemotactic non-chemokine chemerin by CCRL2 to CMKLR1, heterodimerization with CXCR2 [22], or interaction with Toll-Like Receptor 4 (TLR4), which facilitates CCRL2 retainment in the cell surface of tumor-associated macrophages (TAMs) and potentiates further anti-tumor CD8+ T-cell responses [23]. The gene discussed is CXCR2; the disease is neoplasm.