In another study, researchers explored and supplemented that CCL5 secreted by macrophages inhibit the CD8+ T-cell-mediated killing behavior of HT29 cells and promote immune escape by activating the p65/STAT3/CSN5 signaling axis to deubiquitinate and stabilize PD-L1, which may form a positive feedback loop and boost the infiltration of macrophages, subsequently promoting the growth of CRC (78). The gene discussed is STAT3; the disease is colorectal carcinoma.