Proteomic studies have revealed that periplakin is aberrantly expressed in esophageal cancer and may be closely associated with lymphatic metastasis.[44] Furthermore, periplakin overexpression has been shown to promote cell lamination, facilitate cell and extracellular matrix adhesion, and retard cell migration, consistent with the trend of low periplakin expression observed in esophageal cancer.[45]. The gene discussed is PPL; the disease is esophageal cancer.