Liu and colleagues showed that, in AML, Bortezomib blocked the binding of Sp1 (Sp1 transcription Factor)/NF-κB complex to the DNA methyl-transferase 1 (DNMT1) gene promoter, leading to a reduced DNA methyltransferase activity that, in turn, induced DNA hypomethylation and silenced gene transcription. Here, NFKB1 is linked to acute myeloid leukemia.