Investigators from Mayo Clinic have shown that EZH2 is recruited to the silenced FOXP3 promoter through a polycomb response element.61 The same group of investigators from Mayo Clinic have also shown that EZH2 deficiency in FOXP3+ cells in mice resulted in multiorgan immunity and decreased survival.62 These mice developed spontaneous IBD. This evidence concerns the gene FOXP3 and inflammatory bowel disease.