Blocking the NF-κB pathway by Ad.IκBαSR resulted in suppressed constitutive and TNFα-induced NF-κB activity and increased sensitivity to pro-apoptotic stimuli in vitro, both in normal human macrophages and in RA synovial cell cultures and macrophages [34,43,89]. This evidence concerns the gene NFKB1 and rheumatoid arthritis.