Considering the involvement of NF-κB pathway on the production of these pro-inflammatory mediators, we focused on the possibility that BJe may regulate NF-κB activation and examined underlying mechanisms associated with NF-κB/SIRT1 crosstalk in LPS-stimulated THP-1 monocytes, a human leukemia monocytic cell line, that have been widely used as a model to study the inflammatory cell response. This evidence concerns the gene NFKB1 and leukemia.