Taken together, these data suggested that Wnt/β-catenin signaling mediated the hypoxia-induced reactivation of Id2 expression and consequently, the enhanced level of Id2 promoted the self-renewal potential of CSCs and tumor metastasis/dissemination as a downstream effector of hypoxia-induced Wnt/β-catenin signaling during colorectal-cancer development. The gene discussed is ID2; the disease is neoplasm.