EMT was promoted, activating invasion, and resulting in elevated PTK6 expression with E-cadherin (E-cad) suppression [10], which is deleted in esophageal cancer 1 (DEC1) upregulation, leading to focal adhesion kinase/serine/threonine kinase (FAK/AKT) [49], and through the upregulation of keratin 17 (Krt17) [52] in murine models. Here, MARK2 is linked to cancer.