Experimental studies utilizing A20myel-KO mice reveal that neither NF-κB inhibition via IKK2 deletion nor TNFR1 ablation fully prevents arthritis, suggesting redundant inflammatory pathways, such as TLR3/TLR4-TRIF or IFN receptor signaling, may compensate to sustain disease progression (41, 72). The gene discussed is NFKB1; the disease is Arthritis.