These effects are not completely surprising since different transcription factors modulated by CCR1 and CCR5,40–42 such as C/EBPβ or STAT3, play important roles in the polarization of multiple myeloid cell subsets including MDSCs, macrophages, and DCs.28 43–46 This can also explain why the targeted silencing of CCR1 and CCR5 affects tumor growth across multiple models even when PMN-MDSCs are not the most abundant protumoral myeloid cells like, for example, the MCA203 model. The gene discussed is CCR5; the disease is neoplasm.