H. pylori infection, a major known risk factor for GC [8,9], and mutations of genes such as adenomatosis polyposis coli (APC), which are present in approximately 70% of patient with intestinal-type gastric adenoma [1,10], are known to activate the Wnt/β-catenin pathway, which is associated with the development and progression of GC. Here, APC is linked to gastric cancer.