Dysplasia carries a high risk of cancer development, however, the cellular mechanisms for dysplasia evolution to cancer are obscure. We have previously identified two putative dysplastic stem cell (DSC) populations, CD44v6neg/CD133+/CD166+ (DP) and CD44v6+/CD133+/CD166+ (TP), which may contribute to cellular heterogeneity of gastric dysplasia. Here, we investigated functional roles and cell plasticity of non-cancerous Trop2+/CD133+/CD166+ DSCs initially developed in the transition from pre-cancerous metaplasia to dysplasia in the stomach.