Furthermore, activation of the TLR/MyD88/NF-κB signaling pathway has been shown to drive the progressive development of multiple SLE-associated phenotypes in mouse models, including splenomegaly, elevated circulating immune complexes, and increased production of pathogenic antinuclear antibodies (ANAs) and anti-dsDNA autoantibodies [222]. The gene discussed is MYD88; the disease is systemic lupus erythematosus.