In this light, N-glycosylated POMK has been evidenced to interact with signaling proteins (other than α-DG) to inhibit the AKT/GSK-3β/Snail metastatic/EMT pathway in breast cancer cells [119] preventing (i) GSK-3β activation and ensuing β-catenin accumulation in the cytoplasm with subsequent nuclear translocation [153], and (ii) Snail stabilization promoting E-cadherin downregulation and adult EMT [103, 119]. This evidence concerns the gene POMK and breast cancer.