HMGB1 and neoplasm: In line with previous report,[20] RA induced markedly apoptosis in MC38 and B16 cells (Figure S1A, Supporting Information), while blockade of apoptosis by a pan‐caspase inhibitor (Z‐VAD‐FMK), but not necroptosis inhibitor (necrostatin1) or lysosomal cell death inhibitor CA‐074 Me, inhibited RA‐induced HMGB1, ATP release and CRT surface expressions in tumor cells (Figure S1B–G, Supporting Information), indicating RA triggered ICD effects of tumor cells mainly through induction of apoptosis.