To dissect the molecular mechanisms of how CD4+ T cells alter chemosensitivity of PCa, we focused on the STAT3 signals, which have demonstrated that constitutively activated phosphorylation of STAT3 (P‐STAT3) contributed to the development of tumor growth, drug resistance, and angiogenesis.17, 18 In addition, the P‐STAT3 signaling pathway can be activated via chemokines or cytokines, such as CCL5.17, 18, 19, 20, 21 P‐STAT3 was increased in PCa cells after coculture with CD4+ T cells, the similar results were obtained in C4‐2 and CWR22RV1 cells with CCL5 treatment (Figure 5A). The gene discussed is STAT3; the disease is neoplasm.