For instance, in prostate cancer models, secretion of CCL5, activation of STAT3, and upregulation of the transcription factor Nanog resulted in chemotherapeutic drug resistance, whereas secretion of CXCL12 and activation of CXCR4 by TAMs occurred following combined docetaxel/androgen deprivation therapy in cases of castration-resistant prostate cancer tumors with poor response (84, 103, 159). This evidence concerns the gene STAT3 and prostate carcinoma.