CTLA4 and cancer: They activate CD103+ dendritic cells and expand TNF-α and iNOS-producing myeloid subsets, enhancing the therapeutic efficacy of dual PD-1/CTLA-4 blockade in cancer immunotherapy.304 Therefore, gaining insight into these resistance mechanisms is essential for optimizing the effectiveness of CTLA-4 inhibitors and for developing combination therapies that can more effectively target multiple immune evasion pathways.