During inflammation, the FOXP3+ T cells rise in order to counterbalance the T effector responses but their inability to abrogate the intestinal inflammation suggests that either they have lost their suppressive capability [27] or they have gained the potential to differentiate into Th17 cells [29].However there is a lot of discrepant data with another study by Makita et al stating that the functional studies of Tregs isolated from IBD patients have similar suppressive capability as the Tregs isolated from control individuals [30]. Here, FOXP3 is linked to inflammatory bowel disease.