Gene network analysis in isolated intestinal CD4+ T cells from patients with CD demonstrated that these CD4+ T cells displayed a Th1/Th17-like phenotype with enrichment of gene targets shared by FOXP3 and EZH2, suggesting that deregulation of FOXP3/EZH2 T cell gene networks in Crohn’s disease could contribute to the underlying intestinal inflammation [186]. Here, FOXP3 is linked to Crohn disease.