No significant changes in the expression of IL-10 were found in natural Treg cells of the IBD model from K2P5.1−/− mice (Figure 5C); however, the long-lasting dysregulation of Ca2+ signaling elicited by a K2P5.1 deficiency may be compensated by the upregulation of other K+ channel(s), and, thus, the expression of IL-10 may be maintained within normal ranges in the Treg cells of the IBD model from K2P5.1−/− mice. This evidence concerns the gene IL10 and inflammatory bowel disease.