Mismatch repair‐deficient tumors induce stronger DC‐mediated cross‐activation of CD8+ T cells, and increased DNA sensing in tumor cells, therefore promoting adaptive immunity.[37] In various treatment environments such as chemotherapy, radiotherapy, and DNA repair pathway‐targeted therapy, damaged DNA enhances T cell activation and antitumor effects by triggering Toll‐like receptors or cGAS‐STING‐dependent IFN‐I signaling.[38, 39] Radiation‐induced activation of cGAS‐STING in DCs is essential for tumor suppression in the immune‐tolerant microenvironment of the liver. The gene discussed is CGAS; the disease is neoplasm.