In the active phase of UC, particularly in the context of Epstein–Barr virus infection, there is a marked decrease in the expression of Foxp3 in Tregs, which inversely correlates with serum C-reactive protein and Mayo score, suggesting their potential role in UC remission (27, 28), Tregs and Th17 cells, primarily found in the spleen and peripheral blood, are mobilized and transferred to intestinal ulcer sites at UC onset, particularly in Peyer’s patches and the spleen, leading to disrupted homeostasis of Treg and Th17 cells and further promoting inflammation and intestinal damage (29, 30). The gene discussed is FOXP3; the disease is intestinal disorder.