HMGB1 and acute myeloid leukemia: In summary, our findings provide additional insights that HMGB1 contributes to the AML pathogenesis and progression by inhibiting apoptosis, facilitating proliferation, and inducing differentiation arrest of AML cells, acting as a promising therapeutic target in AML, and further demonstrating the therapeutic effect of chidamide on AML by reversing the biological processes correlated with the pathogenesis and progression of AML via downregulating HMGB1 expression.