Since NF-κB has been found constitutively active, both in the blasts and stem cells of acute myeloid leukemia [76], and its activation is detected in the bone marrow of patients with myelodysplastic syndrome (considered a precursor disease of AML [5]), the lack of formation of the NEMO/IKK complex due to the use of NEMO-binding domain peptides could represent a therapeutic strategy to indirectly inhibit NF-κB activation in AML. This evidence concerns the gene IKBKG and myelodysplastic syndrome.