HMGB1 and neoplasm: In a model of in situ ICD, tumor-infiltrating CD103+ cDC1s and CD103- cDC2s showed accelerated turnover within the tumor and emigrated to draining lymph nodes mediated via the ATP/P2X7R and HMGB1/TLR4 signaling pathways, leading to an increased CD8+ T-cell antitumor response and the suppression of secondary tumor growth [196].