In nasopharyngeal carcinoma, PCDH20 was identified as a functional tumor suppressor via inactivation of Wnt/β-catenin signaling and epithelial-to-mesenchymal transition, with frequent epigenetic inactivation observed [19], while another study on HCC revealed that hypermethylation of the PCDH20 promoter accounted for its downregulation; moreover, overexpression of PCDH20 could inhibit cell proliferation and cell migration by antagonizing the Wnt/β-catenin signaling pathway [20]. Here, PCDH20 is linked to neoplasm.