We have published data sets revealing the majority of FOXP3 gene targets in CD4+ lymphocytes isolated from Crohn’s lesions are significantly up-regulated. FOXP3 gene target status in the disease state is incongruent with FOXP3 and its associated complex functioning as an established gene repressor/silencer. This finding of up-regulated gene expression is best explained by the gain of a co-activation complex in addition to loss of repression. A putative FOXP3 co-activator complex associated with Crohn’s disease is unknown.