Prior studies in humans with STAT3 GOF syndrome suggest that these patients may have defects in FOXP3+ Tregs; this is based on studies demonstrating reduced Treg frequency in the peripheral blood of patients, organ-specific autoimmunity (i.e., enteropathy, type 1 diabetes, cytopenias), and in some instances, reduced Treg suppressive capacity in vitro (10, 14, 15, 21, 22). This evidence concerns the gene STAT3 and Abnormal intestine morphology.