The main results of the present study were as follows: (1) Facilitation of the expression level and functional activity of the K2P5.1 K+ channel in splenic CD4+ T cells of IBD model mice, especially in the CD4+CD25− subset (Figures 1, 2), (2) Decreased disease activity index (diarrhea, bloody feces, and weight loss) and histopathological scores (colonic inflammation and crypt damage) in homozygous K2P5.1-deficient (K2P5.1−/−) mice (Figure 4). The gene discussed is KCNK5; the disease is inflammatory bowel disease.