In both the mouse and human literature, TNFR2-expressing Tregs have been shown to be the most suppressive Tregs identified to date.6, 9, 13 Also TNFR2 is required for potent Treg function and disease suppression in animal models of multiple sclerosis such as the EAE mouse model.36 aTregs are normally maintained through transmembrane forms of TNF (tmTNF) yet T1D have normal levels of tmTNF so the mechanism behind the paucity of aTregs in T1D is unknown (data not shown). The gene discussed is TNFRSF1B; the disease is multiple sclerosis.