To explore a broader utilization of our finding in other cancer types, particularly ICB-responsive models, we knocked out C/EBPβ in murine EO771 and human MDA-MB-231 breast cancer cells and showed that the KO of C/EBPβ could markedly enhance chemokine expression and promote the tumor infiltration of T cells, which, in turn, enhances the efficacy of PD-1 Ab immunotherapy. The gene discussed is PDCD1; the disease is breast carcinoma.