Its upregulation on DCs by factors present in the TME seems to be an important mechanism by which TADCs are locked into an immune-suppressive phenotype, preventing the detection of tumor-derived danger signals through an interaction with the DAMP molecule, high mobility group box 1 (HMGB1), and leading to the release of immune-suppressive factors, with consequent attenuation of the therapeutic efficacy of DNA vaccination and chemotherapy in experimental tumor models [130]. This evidence concerns the gene HMGB1 and neoplasm.