Specific ablation of TNFR2 in Tregs did not decrease their numbers but diminished expression of signature genes and impaired suppressive activity in vitro, and in vivo in an experimental autoimmune encephalitis model, directly demonstrating a critical intrinsic role of TNFR2 to maintain the functionality of Treg cells [82]. The gene discussed is TNFRSF1B; the disease is autoimmune encephalitis.