Using transgenic mice that overexpress β-catenin agonist Wnt1, Oguma et al. observed that H. pylori infection lead to rapid infiltration of macrophages within dysplastic mucosa in close apposition to gastric epithelial cells and suggested that macrophage derived TNF promotes Wnt/β-catenin signaling, which may contribute to tumor development in gastric mucosa [37]. This evidence concerns the gene TNF and neoplasm.