HMGB1 and neoplasm: TNBCs, as a “cold” tumor, severely limited the efficiency of ICB therapy, while chidamide (CHI), a selective HDACi, enhanced the antitumor immunoreactivity of ICB treatment by inducing ICD, including calreticulin (CRT) eversion, high mobility group box 1 (HMGB1) release, and adenosine triphosphate (ATP) secretion.