Prior studies demonstrated that most MDS and AML patients are especially dependent on IL-1 and an IL-1-rich environment, promoting the expansion of malignant progenitors while suppressing normal progenitors [40,41] After cytokine blockade e.g., by monoclonal antibodies, the inhibition of erythroid progenitor colony-forming capacity should be interrupted, resulting in a reactivation of erythropoietin gene expression and improvement of anemia [42]. The gene discussed is EPO; the disease is anemia.