CSF3 and acute myeloid leukemia: The rationale for the regimen includes: (1) G-CSF priming has been found to preferentially potentiate Ara-C and anthracycline- mediated cytotoxicity on AML cells and AML progenitor cells (CFU-AML), presumably by enhancing G0 resting AML cells into the cell cycle [15]; (2) prolonged exposure to low-dose Ara-C and G-CSF can lead to preferential killing of CFU-AML [16]; (3) Aclarubicin is effective regardless of multi-drug resistance gene status [17]; (4) CAG combination may inhibit the self-renewal capacity of CFU-AML and leukemia stem cells [18].