For example, effector T cells from RRMS patients with active disease are resistant to suppression by FoxP3-Treg cells, which is mediated by an increase in IL-6 signaling and downstream activation of signal transducer and activator of transcription (STAT)3.244 In parallel, a subset of self-antigen-specific Treg cells lost the expression of FoxP3 in the context of autoimmunity activation in the EAE model, supporting the notion that, in MS, the immunoregulatory function of Treg cells is impaired and fails to control the autoimmune process.245. This evidence concerns the gene FOXP3 and Autoimmunity.