Foxp3 gene, fewer T cells are observed. The remaining T cells have poor proliferative and cytolytic responses and poor interleukin-2 production, although thymic development appears normal. Histologic analysis indicates that peripheral lymphoid organs, particularly lymph nodes, lack the proper number of cells. Role in cancer In addition to Foxp3's role in regulatory T cell differentiation, multiple lines of evidence have indicated that Foxp3 play important roles in cancer development. Down-regulation of Foxp3 expression has been reported in tumour specimens derived from breast, prostate, and ovarian cancer patients, indicating that Foxp3 is a potential tumour suppressor gene. Expression of Foxp3 was also detected in tumour specimens derived from additional cancer types, including pancreatic, melanoma, liver, bladder, thyroid, cervical cancers. However, in these reports, no corresponding normal tissues was analyzed, therefore it remained unclear whether Foxp3 is a pro- or anti-tumourigeneic molecule in these tumours. Two lines of functional evidence strongly supported that Foxp3 serves as tumour suppressive transcription factor in cancer development. First, Foxp3 represses expression of HER2, Skp2, SATB1 and MYC oncogenes and induces expression of tumour suppressor genes P21 and LATS2 in breast and prostate cancer cells. Second, over-expression of Foxp3 in melanoma, glioma, breast, prostate and ovarian cancer cell lines induces profound growth inhibitory effects in vitro and in vivo. However, this hypothesis need to be further investigated in future studies. Foxp3 is a recruiter of other anti-tumor enzymes such as CD39 and CD8. The overexpression of CD39 is found in patients with multiple cancer types such as melanoma, leukemia, pancreatic cancer, colon cancer, and ovarian cancer. This overexpression may be protecting tumorous cells, allowing them to create their “escape phase”. A cancerous tumor's “escape phase” is where the tumor grows quickly and it becomes clinically invisible by becoming independent of the extracellular matrix and creating its own immunosuppressive tumor microenvironment. The consequences of a cancer cell reaching the “escape phase” is that it allows it to completely evade the immune system, which reduces the immunogenicity and ability to become clinically detected, allowing it to progress and spread throughout the body. Some cancer patients have also been known to display higher numbers of mutated CD4+ cells. These mutated cells will then produce large quantities of TGF-β and IL-10, (a Transforming Growth Factor β and an inhibitory cytokine respectively,) which will suppress signals to the immune system and allow for tumor escape. So, Foxp3 polymorphism (rs3761548) might contribute to