Importantly, the increased presence of Helicobacter in Pla2g2a–/– mice could explain why mouse strains with a mutated Pla2g2a gene are more prone to intestinal tumorigenesis than those with a native Pla2g2a gene (28), why Tg transfer of the Pla2g2a gene into Pla2g2a-null C57BL/6 mice reduces the incidence of intestinal polyposis (72), and why PLA2G2A expression is inversely correlated with gastric cancer in humans (73). The gene discussed is PLA2G2A; the disease is gastrointestinal polyp.