GZMA and autoimmune disease: The major function of JunB in Tregs is to maintain CD25− Treg cells—perhaps by facilitating metabolic adaptation—and to drive expression of a subset of genes in the colon including granzymes A and B. Remarkably, despite largely normal expression of most Treg effector genes, loss of the JunB-dependent subset of the Treg transcriptome is sufficient to cause spontaneous immune dysregulation, suggesting that impairment of organ-specific Treg effector mechanisms may drive development of autoimmune disease.