The elevated level of nuclear β-catenin and Wnt signaling in these tumors may be due to high expression of Wnt factors in the tumor environment, loss of APC, Wnt inhibitors (DKK1, SFRPs), and/or E-cadherin expression by epigenetic modification/gene silencing, or alterations in the expression of other genes that encode constituents of the pathway (RSPO2, FZD6) [27]. Here, DKK1 is linked to neoplasm.