Our previous study had shown that CCL5 could modulate the differentiation of MDSCs to promote tumor progression in luminal and triple-negative breast cancer.22, 38And in CRC model, CCL5-deficiency inhibited tumor growth and metastasis by resulting in the metabolic disorders in CD11bhiF4/80lowTAMs and suppressing the expression of S100a9 to promote the migration of CD8+T cells in the TME.21All of above studies suggested that CCL5 involved in differentiation of myeloid cells, besides its chemotaxis function. The gene discussed is S100A9; the disease is neoplasm.