While mutations in the FOXP3 gene result in the development of autoimmunity at birth, the seminal studies by the Rudensky lab and others [6, 7, 8] demonstrating that depletion of Foxp3 expressing Treg from adult transgenic mice expressing the diphtheria toxin receptor (DTR) under the control of the Foxp3 promoter (Foxp3‐DTR) also results in the rapid development of a multiorgan inflammatory syndrome establish that Treg plays a critical role in the maintenance of immune homeostasis in the steady state. The gene discussed is FOXP3; the disease is Autoimmunity.