This suggests a potential mechanism where defective Treg function could lead to ongoing autoimmunity, characterized by the loss of FOXP3 expression under inflammatory conditions and induction of proinflammatory cytokines such as IL-17A and IFN-γ (IFN-γ+ FOXP3+ IL-17A+) [31,32,33]. The gene discussed is FOXP3; the disease is Autoimmunity.