Although this study did not address if the CCR2+ CD11b+ cells were MDCSs based on functional assays or definitive MDSC phenotypes (e.g., high level of Arginase 1 expression) and how CCL2 deficiency abrogated Treg accumulation in the tumor, others have reported that TME and MDSCs promote Treg infiltration into tumors by secreting T cell-attracting chemokines [217]. The gene discussed is CCR2; the disease is neoplasm.