Subsequently, the present data provided strong evidence that overexpression of HDAC1 increased doxorubicin resistance of AML cells and that silencing of HDAC1 decreased doxorubicin resistance of AML cells by exerting effects on cell viability, cell apoptosis, the doxorubicin-releasing index, and MRP1 expression. Here, HDAC1 is linked to acute myeloid leukemia.