Two recent studies showed that the embryonic factor netrin-1 exhibited pro-EMT activities, and blocking netrin-1 with a monoclonal antibody inhibited EMT, increased the proportion of epithelial cells, reduced metastasis, and potentiated therapy efficacy in mouse models of skin squamous cell carcinoma and endometrial adenocarcinoma [8,9]. The gene discussed is NTN1; the disease is endometrium adenocarcinoma.