The results of TNFAIP3-deficient unfettered inflammation appears dependent upon cell type and other unknown factors: mice lacking TNFAIP3 specifically in lysozyme M expressing macrophages and granulocytes develop an RA phenotype, whereas mice conditionally deficient for TNFAIP3 in CD11c dendritic cells either develop SLE or manifest more of a spondyloarthritis phenotype, with enthesitis, axial disease, and gut pathology (independent studies performed at different institutions) (5–8). This evidence concerns the gene TNFAIP3 and spondyloarthropathy.