This multi-layered approach appears typical of poxviral control of NF-κB regulation and extends to the poxviral ANK repeat proteins, with the K1L protein inhibiting IκB degradation, [107] and thereby blocking NF-κB signal transduction of viral infection from Toll-like receptors, TLR2, TLR4 and TLR9 [131]. The gene discussed is NFKB1; the disease is viral infectious disease.