The total numbers of splenic and mesenteric IFNγ+ Tregs were significantly higher in NOD.LckCrePrdm1F/F than in their NOD WT littermate controls, but the percentages and total numbers of IFNγ+ Tregs from the spleens and mLNs were comparable between B6.LckCrePrdm1F/F mice and controls (Fig. 3h), supporting the idea of a more fragile phenotype of Blimp-1-deficient Tregs with lower suppressive activity for controlling intestinal inflammation in mice from the autoimmune diabetes-prone background than in non-diabetes-prone mice. Here, IFNG is linked to diabetes mellitus.