Unexpectedly, despite the increased numbers of aTreg cells, Foxp1f/fFoxp3Cre mice gradually develop spontaneous inflammatory diseases with age, and have more severe disease in DSS-induced colitis and EAE models, indicating that, although Foxp1 helps restrain the differentiation of aTreg cells from rTreg cells, it is also important for the suppressive function of aTreg cells. This evidence concerns the gene FOXP1 and colitis.