These findings suggest that TZ‐dSA3‐12 modulates DC‐CD8+T cell immunity for tumor control, aligning with previous reports that EGFR‐targeted STING agonist ADC promotes DCs maturation, antigen cross‐presentation, and CD8+ T cells expansion.[18] Moreover, we observed that the DCs population decreased in the tumors and increased in the dLN following TZ‐dSA3‐12 treatment, suggesting that TZ‐dSA3‐12‐activated DCs likely capture tumor antigens and migrate to dLN, where they prime T cells[27] and induce a long‐term immune memory response. This evidence concerns the gene CD8A and neoplasm.