Increased levels of complex N-glycans with β1,6 N-acetylglucosamine (catalyzed by GlcNAcT-V) on E-cadherin were more recently shown to cause weakening of E-cadherin mediated cell–cell adhesion leading to increased tumor progression [13], and the same study demonstrated that modification of E-cadherin with bisected N-glycans (catalyzed by GlcNAcT-III) increases the stability of adherens junctions and is associated with suppression of tumor progression. The gene discussed is CDH1; the disease is neoplasm.