According to this model, AML cells significantly change the behavior of ECs to produce microenvironments permissive to AML growth, opening new avenues for AML therapy to include agents that prevent EC activation (e.g., anti-TNF-α antibodies, antioxidants, or glucocorticoids), with the aim of reducing NSC adhesion to the protective niche, thereby potentially increasing sensitivity to conventional chemotherapy [127]. This evidence concerns the gene TNF and acute myeloid leukemia.