In melanoma patients, tumor-derived SAA regulated the plasticity of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) through the binding to the Formyl peptide receptor 2 (FPR-2) on the surface of these cells, resulting in the expansion of IL-10-secreting PMN-MDSCs, which downregulated T-cell anti-tumor activity [28]. This evidence concerns the gene FPR2 and neoplasm.