As regards BC, Anticin-A demonstrated the ability to arrest the epithelial-to-mesenchymal transition (EMT) in human estrogen receptor-positive MCF7 and triple-negative MDA-MB-231 cells, acting through the upregulation of the epithelial markers E-cadherin and occludin, and through the concomitant downregulation of the mesenchymal markers N-cadherin and vimentin. The gene discussed is CDH1; the disease is breast cancer.