of a single interleukin. IL-6 or IL-21 is being debated by immunology laboratories as the definitive signaling molecule. Murine studies point to IL-6 whereas human studies have shown IL-21. Foxp3 is the major transcription factor controlling T-regulatory cells (Treg or CD4+ cells). CD4+ cells are leukocytes responsible for protecting animals from foreign invaders such as bacteria and viruses. Defects in this gene's ability to function can cause IPEX syndrome (IPEX), also known as X-linked autoimmunity-immunodeficiency syndrome as well as numerous cancers. While CD4+ cells are heavily regulated and require multiple transcription factors such as STAT-5 and AhR in order to become active and function properly, Foxp3 has been identified as the master regulator for Treg lineage. Foxp3 can either act as a transcriptional activator or suppressor depending on what specific transcriptional factors such as deacetylases and histone acetylases are acting on it. The Foxp3 gene is also known to convert naïve T-cells to Treg cells, which are capable of an in vivo and in vitro suppressive capabilities suggesting that Foxp3 is capable of regulating the expression of suppression-mediating molecules. Clarifying the gene targets of Foxp3 could be crucial to the comprehension of the suppressive abilities of Treg cells. Pathophysiology In human disease, alterations in numbers of regulatory T cells – and in particular those that express Foxp3 – are found in a number of disease states. For example, patients with tumors have a local relative excess of Foxp3 positive T cells which inhibits the body's ability to suppress the formation of cancerous cells. Conversely, patients with an autoimmune disease such as systemic lupus erythematosus (SLE) have a relative dysfunction of Foxp3 positive cells. The Foxp3 gene is also mutated in IPEX syndrome (Immunodysregulation, Polyendocrinopathy, and Enteropathy, X-linked). Many patients with IPEX have mutations in the DNA-binding forkhead domain of FOXP3. In mice, a Foxp3 mutation (a frameshift mutation that result in protein lacking the forkhead domain) is responsible for 'Scurfy', an X-linked recessive mouse mutant that results in lethality in hemizygous males 16 to 25 days after birth. These mice have overproliferation of CD4+ T-lymphocytes, extensive multiorgan infiltration, and elevation of numerous cytokines. This phenotype is similar to those that lack expression of CTLA-4, TGF-β, human disease IPEX, or deletion of the Foxp3 gene in mice ("scurfy mice"). The pathology observed in scurfy mice seems to result from an inability to properly regulate CD4+ T-cell activity. In mice overexpressing the