A study published in *Nature* (2015) challenges the long-held belief that epithelial-to-mesenchymal transition (EMT) is essential for lung metastasis in breast cancer. Using a lineage tracing system, researchers found that lung metastases primarily consist of non-EMT tumor cells that maintain their epithelial phenotype. While EMT does not impact metastasis development, EMT cells contribute to recurrent metastasis after chemotherapy due to reduced proliferation, increased apoptotic resistance, and elevated chemoresistance-related gene expression. Overexpression of miR-200, a known EMT inhibitor, abrogated this resistance. The study suggests that targeting EMT in combination with conventional chemotherapy could improve breast cancer treatment. The findings indicate that EMT is not required for metastasis formation but may play a role in chemoresistance. The research used multiple mouse models to demonstrate that EMT does not significantly contribute to lung metastasis development. The study also highlights the importance of EMT in chemoresistance, showing that EMT cells are more resistant to chemotherapy due to reduced proliferation, increased apoptotic resistance, and upregulated chemoresistance-related genes. These findings suggest that targeting EMT could be a promising strategy for improving chemotherapy outcomes in breast cancer.A study published in *Nature* (2015) challenges the long-held belief that epithelial-to-mesenchymal transition (EMT) is essential for lung metastasis in breast cancer. Using a lineage tracing system, researchers found that lung metastases primarily consist of non-EMT tumor cells that maintain their epithelial phenotype. While EMT does not impact metastasis development, EMT cells contribute to recurrent metastasis after chemotherapy due to reduced proliferation, increased apoptotic resistance, and elevated chemoresistance-related gene expression. Overexpression of miR-200, a known EMT inhibitor, abrogated this resistance. The study suggests that targeting EMT in combination with conventional chemotherapy could improve breast cancer treatment. The findings indicate that EMT is not required for metastasis formation but may play a role in chemoresistance. The research used multiple mouse models to demonstrate that EMT does not significantly contribute to lung metastasis development. The study also highlights the importance of EMT in chemoresistance, showing that EMT cells are more resistant to chemotherapy due to reduced proliferation, increased apoptotic resistance, and upregulated chemoresistance-related genes. These findings suggest that targeting EMT could be a promising strategy for improving chemotherapy outcomes in breast cancer.