ID2 and neoplasm: Taken together, these data suggested that Wnt/β-catenin signaling mediated the hypoxia-induced reactivation of Id2 expression and, consequently, the increased 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 (Fig. 7).