CSF3 and acute myeloid leukemia: Several mechanisms for its high efficacy have been proposed: (1) AML cells transition out of the G0 phase because G-CSF stimulation via cell surface receptors allows the other chemical agents to kill resting leukemic cells; (2) Priming with G-CSF effectively enhances cytarabine-induced apoptosis of AML cells; (3) The addition of G-CSF to the regimen enhances the ability of low doses of cytarabine to induce the differentiation of AML cells; (4) Aclarubicin is effective regardless of multi-drug resistance gene status [9].