Furthermore, lineage tracing studies have confirmed that differentiated cancer cells could revert to LGR5+ CSCs, thus contributing to tumor growth[23] in colorectal cancer, while epigenetic regulation facilitates Lgr5+ intestinal stem cell formation by inducing the dedifferentiation of secretory precursors.[24] Despite these advances, the phenotypic plasticity of tumor epithelium and transcriptional tumorigenic trajectory of gastric CSCs, as well as the mechanism by which the CSC niche induces gastric CSC formation, have not yet been fully elucidated. This evidence concerns the gene LGR5 and neoplasm.