Accumulating evidence indicates that OGT-mediated O-GlcNAcylation on a variety of substrates including transcription factors, oncoproteins, and proteins associated with epithelial mesenchymal transition (EMT) promotes tumor metastatic capacity in numerous cancer cells, including those derived from colorectal cancer (CRC), breast cancer, gastric cancer, pancreatic cancer, and cholangiocarcinoma (CCA) (31, 41–45). The gene discussed is OGT; the disease is breast cancer.