While we can only explain these differences by different methods (mRNA versus flow cytometry) and different AML patient collectives, based on our data we would like to propose a different mechanism for IL-8 in the context of AML: no auto- or parakrine stimulation of AML but instead, modulation of the microenvironment by AML blasts; and while a proangiogenic effect of IL-8 – angiogenesis being microenvironment as well–has been well established30, in our hypothesis, the affected microenvironment would be mesenchymal stromal cells. The gene discussed is CXCL8; the disease is acute myeloid leukemia.