The nuclear factor-κB (NF-κB) signaling pathway plays a major role in the development, maintenance, and progression of most chronic diseases. NF-κB controls the expression of genes involved in a number of physiological responses, including immune inflammatory responses, acute-phase inflammatory responses, oxidative stress responses, cell adhesion, differentiation, and apoptosis [1]. Recent studies have suggested that NF-κB dysregulation is associated with many diseases including AIDS, atherosclerosis, asthma, arthritis, diabetes, inflammatory bowel disease, stroke, muscle wasting and viral infections. Mounting evidence indicates that NF-kB acts as a link between inflammation and cancer progression [2–10], making NF-κB essential to and a potential drug target in hematological malignancies and solid tumors [11, 12]. NF-κB was first identified in 1986 by Sen and Baltimore [5] in the nucleus bound to an enhancer element of the immunoglobulin kappa light chain gene in B cells [5, 13]. It is now known to be ubiquitous in nature present in all the cell types and is evolutionary conserved. It belongs to the family of Rel proteins that includes c-Rel, RelA (p65), RelB, NF-κB1 (p50 and its precursor p105), and NF-κB2 (p52 and its precursor p100) all of which can form hetero- or homodimers [14–16].
