FOXP3 and colitis: CDK2-mediated phosphorylation of Foxp3 at Ser19 and Thr175 negatively modulated its protein stability and transcriptional activity, hence downregulating the function of Treg cells to promote the development of colitis, suggesting that CDK2-mediated and Foxp3-based phosphorylation can modulate the intestinal inflammation [96,97].