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Numerous papers documenting the key clinical and molecular characteristics of IPEX have provided a detailed understanding of this devastating disease. IPEX is a primary immunodeficiency caused by mutations in the gene <jats:italic>FOXP3<\/jats:italic>, which encodes an essential transcription factor required for maintenance of thymus\u2010derived regulatory T (tT<jats:sub>reg<\/jats:sub>) cells. tT<jats:sub>reg<\/jats:sub>\u00a0cell dysfunction is the main pathogenic event leading to multiorgan autoimmunity in IPEX. In addition to the traditional clinical presentation (i.e., severe enteropathy, type 1 diabetes, and eczema), IPEX may encompass other variable and distinct clinical manifestations. As IPEX awareness and characterization have increased, so has identification of <jats:italic>FOXP3<\/jats:italic> mutations, with at least 70 to date. Thus, while <jats:italic>FOXP3<\/jats:italic> is the unifying gene, IPEX is a complex and diverse clinical continuum of disorders. Despite understanding IPEX pathogenesis, new treatment options have remained elusive, although early diagnosis led to hematopoietic stem cell transplantation (HSCT) and immunosuppression treatment and improved patient outcomes. Here, we review current knowledge about IPEX syndrome and highlight findings that could lead to novel targeted treatments.<\/jats:p>","DOI":"10.1111\/nyas.13011","type":"journal-article","created":{"date-parts":[[2016,2,26]],"date-time":"2016-02-26T10:32:05Z","timestamp":1456482725000},"page":"5-22","source":"Crossref","is-referenced-by-count":320,"title":["From IPEX syndrome to <i>FOXP3<\/i> mutation: a lesson on immune dysregulation"],"prefix":"10.1111","volume":"1417","author":[{"given":"Rosa","family":"Bacchetta","sequence":"first","affiliation":[{"name":"Department of Pediatrics Division of Pediatric Stem Cells, Transplantation and Regenerative Medicine Stanford University Medical School  Stanford California."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Federica","family":"Barzaghi","sequence":"additional","affiliation":[{"name":"San Raffaele Telethon Institute for Gene Therapy Division of Regenerative Medicine Stem Cells and Gene Therapy San Raffaele Scientific Institute  Milan Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria\u2010Grazia","family":"Roncarolo","sequence":"additional","affiliation":[{"name":"Department of Pediatrics Division of Pediatric Stem Cells, Transplantation and Regenerative Medicine Stanford University Medical School  Stanford California."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,2,25]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-3476(82)80573-8"},{"key":"e_1_2_12_3_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI11679"},{"key":"e_1_2_12_4_1","first-page":"1379","article-title":"X\u2010linked lymphoreticular disease in the scurfy (sf) mutant mouse","volume":"138","author":"Godfrey V.L.","year":"1991","journal-title":"Am. 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