The STAT5 tetramers were showed to promote the pathogenesis of experimental autoimmune encephalomyelitis, and the production of CCL17 was regulated by GM-CSF-mediated STAT5 tetramerization through monocyte-derived cells in the STAT5 tetramer-deficient N-domain double knockout mouse [32]. Here, STAT5A is linked to experimental autoimmune encephalomyelitis.