Additionally, previous study has reported that CX4945 can improve the TME by downregulating PD‐L1 expression on tumor cells.[22] To further investigate whether CX4945's regulation of CD8+ T cell exhaustion in vivo depends on the reduction of PD‐L1 expression on tumor cells, we established an LLC‐OVA‐transplanted tumor mouse model and restored PD‐L1 expression in tumor tissues by administering chloroquine to counteract the downregulation caused by CX4945. Here, CD274 is linked to neoplasm.