After stimulation and activation of the canonical NF-κB pathway in noncancer cells, IκB is phosphorylated by IKK then degradated by the 26S proteasome allowing the nuclear transport of NF-κB. Since IκB is a substrate of the proteasome, the initial rationale for use of bortezomib in multiple myeloma was inhibition of NF-κB activity and inhibition of cell proliferation and survival [25, 26]. Here, NFKB1 is linked to plasma cell myeloma.