These and other findings support the notion that a coordinated interplay exists between O-mannosyl glycosylation and N-glycosylation positively and negatively modulating, respectively, E-cadherin function, and that loss of the first in favor of the second could lead to loss of E-cadherin suppressive functions in cancer, thus contributing to tumor progression and metastasis [137]. The gene discussed is CDH1; the disease is neoplasm.