FOXP3 and cranioectodermal dysplasia: This isoform compromises the interaction between FOXP3 and transcription factors RORαt and RORγt, thereby promoting Th17 differentiation.312 This shift in FOXP3 isoform expression underscores how the intestinal microenvironment can reprogram Tregs, undermining their capacity to maintain immune tolerance and exacerbating the inflammatory response in CeD.