UHRF1 and colitis: This is complemented by studies by others where loss of uhrf1 is pro-inflammatory: uhrf1 mutant zebrafish have intestinal inflammation associated with cell death that is dependent on tnf a (8), mice with uhrf1 deficient regulatory T-cells develop spontaneous colitis in part due to a loss of the immunomodulatory function of these cells (19) and a recent study showing that deleting uhrf1 in mature T-regulatory cells leads to spontaneous inflammation in multiple organs and the acquisition of a pro-inflammatory gene expression pattern, counteracting the immunosuppressive function (20).