Recently Foxp3+ Tregs have been shown to aid in epithelial repair in experimental colitis, and Treg cell suppression or dysfunction is known to accelerate lesion formation in clinical IBD.[34, 35, 36] Thus, HIF‐1α‐orchestrated recruitment of Tregs to active ulcers may directly contribute to healing in DPCA‐treated mice. This evidence concerns the gene HIF1A and inflammatory bowel disease.