Development of new therapeutic strategies utilizing the survival (NF-kB, STAT, PI3 kinase, PTEN, p53) and self-renewal (Wnt, Hedgehog, Notch) pathways for the eradication of these dormant LSCs has critical therapeutic importance for the ultimate goal of cure for AML (Fig. 1). This evidence concerns the gene NFKB1 and acute myeloid leukemia.