It was reported that translocated β-catenin to the nucleus through canonical Wnt signaling directly interacted with Tcf3 to repress pluripotency transcription factors [51], and, in gastric cancer cells, Helicobacter pylori activated Wnt/ β-catenin signaling which, in turn, upregulates Nanog and Oct4 to promote CSC-like properties [52]. This evidence concerns the gene NANOG and gastric cancer.