Nuclear factor kappa B (NF-kB) is a family of inducible transcription factors that orchestrate the expression of genes governing inflammation, innate and adaptive immunity, cell survival, and proliferation. In resting cells, NF-kB dimers, most commonly the prototypical p65 (RelA)/p50 heterodimer, are sequestered in the cytoplasm through association with inhibitory IkB proteins, of which IkB-alpha is the best characterized. Stimulation by proinflammatory cues such as TNF, IL-1, or microbial products triggers the IkB kinase (IKK) complex, whose catalytic subunit IKK-beta phosphorylates IkB-alpha. Phosphorylated IkB-alpha is rapidly polyubiquitinated and degraded by the proteasome, liberating NF-kB dimers to translocate into the nucleus. Once nuclear, phosphorylation of p65 on serine residues enhances its transactivation potential and association with coactivators, driving transcription of cytokines, chemokines, adhesion molecules, and antiapoptotic genes. The p50/NF-kB1 subunit, generated by processing of the p105 precursor, contributes both activating and repressive dimers, while c-Rel selectively governs lymphocyte activation, immunoglobulin class switching, and regulatory T-cell programs. Because unrestrained NF-kB activity is deleterious, the pathway is tightly autoregulated. Newly synthesized IkB-alpha resequesters NF-kB, and the deubiquitinating enzyme and ubiquitin-editing protein A20/TNFAIP3 terminates signaling by disassembling ubiquitin scaffolds upstream of IKK, acting as a critical brake whose loss is linked to autoimmune and inflammatory disease. Dysregulated NF-kB signaling underlies chronic inflammation, autoimmunity, and many lymphoid and epithelial malignancies, making the components of this cascade central targets for therapeutic intervention. Studying the dynamic phosphorylation, degradation, and nuclear translocation of these molecules requires reagents that distinguish total from phosphorylated species. This sampler pack brings together validated antibodies against NF-kB p65, Phospho-NF-kB p65, IkB-alpha, Phospho-IkB-alpha, IKK-beta, p50/NF-kB1, c-Rel, and A20/TNFAIP3 for studying canonical NF-kB pathway activation and its regulation.