TIM-1 knockout experiments showed that expBreg were dependent on TIM-1 to modulate STAT3 phosphorylation and control suppressive potency.1 When phosphorylated upon activation by a variety of stimuli including IL-10, IL-21, and CD40L, pSTAT3 translocates from the cytoplasm to nucleus, where it binds to the IFN-γ–activated sequence in target promoters and activates transcription, including that of IL-10.63 The importance of this pathway in Breg function is illustrated in autoimmune disease. This evidence concerns the gene IL10 and autoimmune disease.