Although the exact protective mechanisms of H. pylori against IBD remain to be fully elucidated, evidence from murine models highlights regulated Th17/Treg cell responses, modulation of NLRP12 expression, and decreased levels of pro‐inflammatory mediators such as COX‐2, TGF‐β, TNF‐α, and tissue transglutaminase (t‐TG) as plausible explanations. The gene discussed is TGM2; the disease is inflammatory bowel disease.