By inhibition of Runx1 in MCF10A (normal) and MCF7 (epithelial like breast cancer) cells, together with re-expression in MCF10AT1 (malignant cells with low Runx1 levels), we provide direct evidence that loss of Runx1 directly contributes to the initiation of EMT in breast cancer, while the presence of Runx1 restores the epithelial phenotype. This evidence concerns the gene RUNX1 and breast carcinoma.