To summarize, CCL28 can alter the proliferation of primary human AML cells for a considerable number of patients, this effect is highly dependent on the local cytokine network and the presence of hematopoietic growth factors, and exogenous CCL28 altered either autocrine or cytokine-dependent (GM-CSF, Flt3L, and SCF) proliferation for 36 of the 56 patients. This evidence concerns the gene FLT3LG and acute myeloid leukemia.