The results of this study, including FACS analysis of myeloid cell populations, RNAseq, and depletion of Ly6G+ cells suggest that the combination of CXCR1/2 inhibition and docetaxel treatment may have either altered the balance of suppressive and anti-tumor myeloid cell populations, or promoted the reprogramming of immature, suppressive myeloid populations into a more anti-tumor phenotype. The gene discussed is CXCR1; the disease is neoplasm.