Given the importance of STAT3 in MDSC expansion and activation32, silencing of STAT3 in PMN-MDSCs via an antisense oligonucleotide tethered to CpG oligonucleotide (CpG-STAT3ASO) reduced circulating PMN-MDSCs and promoted the CTL to Treg ratio in prostate cancer models53. This evidence concerns the gene STAT3 and prostate carcinoma.