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Checkpoint inhibitors best perform in neoadjuvant settings for a number of solid malignancies including cutaneous melanoma as compared with adjuvant schemes. A key difference between both treatment settings is the availability of tumor antigens to continuously prime antitumor T lymphocytes. Mounting evidence indicates that priming is a function chiefly performed by a subset of dendritic cells that cross-present tumor antigens rather than by malignant cells themselves. Acting in favor of these mechanisms to foster tumor-antigen priming is proposed to enhance the efficacy of adjuvant schemes.