The importance of Treg cells in forestalling autoimmunity has been most vividly demonstrated by wide-ranging clinical manifestations of human monogenic disorders resulting from Treg deficiency or dysfunction due to FOXP3, STAT5B, IL2RA, and LRBA mutations or CTLA4 haplo-insufficiency46, 47. This evidence concerns the gene CTLA4 and hyperinsulinemic hypoglycemia, familial, 4.