PRF1 and neoplasm: As an example, inhibition of CCL2 produced by MDSCs, inhibits JAK/STAT3 pathway and reduces MDSC trafficking to the site of tumor (82), while targeting STAT3 in tumor-bearing mice, exhibits a higher expression of the NK activation markers NKG2D, CD69, Fas ligand (FasL), granzyme B, perforin, and IFNγ, resulting in reduced tumor growth (38, 83).