Helicobacter pylori, which is an important cause for gastric cancer, activates β-catenin signaling in multiple ways including affecting the expression of Wnt ligands [52], activating Wnt receptors [53], suppressing GSK3β [54,55], interfering with β-catenin/TCF4 complex by downregulating the gastric tumor suppressor Runx3 [56–58], and interacting with E-cadherin to disrupt the E-cadherin/β-catenin complex [59]. Here, TCF4 is linked to neoplasm.