Notably, recent studies have not only shown that in vivo depletion of FOXP3+ Treg cells in H. pylori-infected mice leads to increased gastric inflammation and reduced bacterial colonization (199), but also recruitment of FOXP3+ Treg cells is increased in H. pylori-related human disorders including gastritis (200, 201), duodenal ulcer (202), and GC (200, 203, 204), suggesting that FOXP3+ Treg cells might contribute to lifelong persistence of H. pylori infection. This evidence concerns the gene FOXP3 and inflammation.