While our principal finding is that overactivity of canonical NF-κB results in the expansion of a pathological subset of Tregs, our model is also remarkable for the pattern of pathology, which by both distribution of inflammation, histopathological analysis and skin transcriptome, exhibits hallmarks of psoriasis in heterozygous mice, and psoriatic arthritis in the homozygous state. The gene discussed is NFKB1; the disease is psoriasis.