Epithelial-mesenchymal transition (EMT) is a process by which epithelial cells lose their polarity and adhesion properties, acquiring a mesenchymal phenotype. This process is crucial in development, tissue repair, and cancer metastasis. The authors propose that EMT can be classified into three subtypes based on the context and outcomes of the transition. Type 1 EMT occurs during embryogenesis, involving the transformation of primitive epithelial cells into mesenchymal cells that later form secondary epithelial cells or undergo apoptosis. Type 2 EMT involves the conversion of secondary epithelial or endothelial cells into fibroblasts, often in response to persistent inflammation. Type 3 EMT is associated with cancer metastasis, where epithelial tumor cells transition into motile metastatic cells. The authors emphasize the importance of using a combination of biomarkers to identify and study EMT events. Key biomarkers include E-cadherin, vimentin, β-catenin, and fibroblast-specific protein 1 (FSP1). Changes in these markers help distinguish between different types of EMT and provide insights into the underlying mechanisms. Additionally, transcription factors such as Snail, Twist, and FOXC2 play critical roles in regulating EMT. Epigenetic modifications and microRNAs, such as those in the miR-200 family, also influence EMT processes. The study highlights the plasticity of epithelial cells and their ability to transition into different cell types under various conditions. Understanding the molecular mechanisms of EMT is essential for developing therapeutic strategies targeting cancer metastasis and fibrosis. The authors suggest that a comprehensive approach, combining multiple biomarkers and considering the context of the transition, will enhance the study of EMT and its implications in disease.Epithelial-mesenchymal transition (EMT) is a process by which epithelial cells lose their polarity and adhesion properties, acquiring a mesenchymal phenotype. This process is crucial in development, tissue repair, and cancer metastasis. The authors propose that EMT can be classified into three subtypes based on the context and outcomes of the transition. Type 1 EMT occurs during embryogenesis, involving the transformation of primitive epithelial cells into mesenchymal cells that later form secondary epithelial cells or undergo apoptosis. Type 2 EMT involves the conversion of secondary epithelial or endothelial cells into fibroblasts, often in response to persistent inflammation. Type 3 EMT is associated with cancer metastasis, where epithelial tumor cells transition into motile metastatic cells. The authors emphasize the importance of using a combination of biomarkers to identify and study EMT events. Key biomarkers include E-cadherin, vimentin, β-catenin, and fibroblast-specific protein 1 (FSP1). Changes in these markers help distinguish between different types of EMT and provide insights into the underlying mechanisms. Additionally, transcription factors such as Snail, Twist, and FOXC2 play critical roles in regulating EMT. Epigenetic modifications and microRNAs, such as those in the miR-200 family, also influence EMT processes. The study highlights the plasticity of epithelial cells and their ability to transition into different cell types under various conditions. Understanding the molecular mechanisms of EMT is essential for developing therapeutic strategies targeting cancer metastasis and fibrosis. The authors suggest that a comprehensive approach, combining multiple biomarkers and considering the context of the transition, will enhance the study of EMT and its implications in disease.