It has been shown in mouse cancer models and using STAT3+ PMN-MDSCs of prostate cancer patients that CpG-siSTAT3 conjugates mediate selective delivery of silencing siSTAT3 to TLR9+ myeloid cells, resulting in disruption of the STAT3 supported suppressive signaling network and stimulation of anti-tumor immunity. This evidence concerns the gene STAT3 and prostate carcinoma.