CDH1 and neoplasm: The phosphorylation of E-cadherin by SYK also phosphorylates the key tyrosine residues involved in the interaction of Hakai with E-cadherin, but SYK and Hakai do not interact; instead, the phosphorylation of E-cadherin by SYK enhances its interaction at adherens junctions with p120-catenin, also inhibiting cell migration and tumor invasion [45].