Indeed, several studies showed that the failure of Foxp3 to associate with TIP60 and HDAC7 leads to altered Foxp3-dependent transcription (higher promoter activity and production of IL-2) and epigenetic modifications, limiting nTreg function at inflammatory sites and decreasing the Treg population in peripheral immune organs, consequently resulting in accelerated fatal autoimmune disease (133, 136, 137). Here, FOXP3 is linked to autoimmune disease.