Our previous studies using genetic STAT3 deletion in tumor-infiltrating myeloid cells or using CpG-STAT3ASO in prostate cancer models suggested that TLR9 activation/STAT3 inhibition results in the recruitment of CD11b+Gr1+ myeloid cells representing not MDSCs but neutrophils, which can contribute to antitumor effects (24, 31). The gene discussed is ITGAM; the disease is neoplasm.