Interestingly, the ABIN1[D485N] knock-in mice spontaneously developed an autoimmune disease similar to Type III and Type IV systemic lupus erythematosus (SLE) in humans, which can be prevented by crossing the ABIN1[D485N] mice to MyD88 KO mice.57 This demonstrates that enhanced MyD88 signalling causes the disease. The gene discussed is MYD88; the disease is autoimmune disease.