A perplexing observation in Crohn’s disease has been the detection of increased numbers of FOXP3+ cells within the lesions, a higher proportion of FOXP3+to CD4+ cells within the mucosa of Crohn’s patients and a significantly higher gene count of FOXP3 from CD4+ cells isolated from lesions. These FOXP3+ cells appear to be unable to suppress inflammation in situ, and their role in disease is poorly understood. We have shown that a majority of FOXP3 gene targets in CD4+ lymphocytes isolated from Crohn’s lesions are in fact significantly upregulated and display a Th1/Th17-like gene set enrichment.