Their activation results from the degradation of IκB proteins, freeing NF-κB to allow their translocation to the nucleus and binding to the target gene promoters (55) To study the role of O-GlcNAcylation on NF-κB signaling in AML, we inhibited O-GlcNAcylation in OCI-AML3 cells that show constitutive NF-κB activity (56). This evidence concerns the gene RUNX2 and acute myeloid leukemia.