The tumor microenvironment in glioblastoma is often characterized by the infiltration of immunosuppressive macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC). High gene expression levels of the chemokine CCL2 are associated with significantly reduced overall survival in glioblastoma patients. Using double-immunofluorescence labeling of glioblastoma patient samples, tumor-infiltrating macrophages were identified as a source of CCL2. Follow-up mechanistic studies in murine gliomas found that macrophage-derived CCL2 recruits Treg cells and monocytic MDSCs through CCR4- and CCR2-dependent interactions, respectively. For details, see article by Chang and colleagues on page 5671.