NFKB1 and acute myeloid leukemia: For example, treating AML cells with the proteasome inhibitor MG-132 increased the amount of phosphorylated IκBα, leading to a strong inhibition of NF-κB activity, decreased expression of NF-κB gene targets and induction of apoptosis in AML cells (including LSCs).13 Importantly, normal hematopoietic stem cells (HSCs), which are not reliant upon NF-κB activity, were spared from this effect.13 These results were amplified when MG-132 was combined with the anthracycline idarubicin.