The article "Molecular mechanisms of epithelial-mesenchymal transition" by Samy Lamouille, Jian Xu, and Rik Derynck, published in *Nature Reviews Molecular Cell Biology*, provides a comprehensive overview of the molecular processes underlying epithelial-mesenchymal transition (EMT). EMT is a critical process in development, wound healing, and stem cell behavior, but it can also contribute to fibrosis and cancer progression. The authors highlight the key transcription factors involved in EMT, including SNAIL, ZEB, and basic helix-loop-helix (bHLH) transcription factors, and their roles in regulating gene expression and cell behavior. They also discuss the signaling pathways that control EMT, such as the TGFβ family, which plays a predominant role in this process. The article covers the deconstruction of cell junctions and polarity, cytoskeletal changes, and the remodeling of the extracellular matrix (ECM) during EMT. Additionally, it explores the role of alternative splicing and microRNAs in regulating gene expression and EMT progression. The authors also review the involvement of tyrosine kinase receptors and growth factors in inducing EMT, emphasizing the roles of PI3K-AKT, ERK MAPK, p38 MAPK, and JNK pathways. Overall, the article provides a detailed and integrated view of the molecular mechanisms underlying EMT, highlighting its significance in various biological and pathological contexts.The article "Molecular mechanisms of epithelial-mesenchymal transition" by Samy Lamouille, Jian Xu, and Rik Derynck, published in *Nature Reviews Molecular Cell Biology*, provides a comprehensive overview of the molecular processes underlying epithelial-mesenchymal transition (EMT). EMT is a critical process in development, wound healing, and stem cell behavior, but it can also contribute to fibrosis and cancer progression. The authors highlight the key transcription factors involved in EMT, including SNAIL, ZEB, and basic helix-loop-helix (bHLH) transcription factors, and their roles in regulating gene expression and cell behavior. They also discuss the signaling pathways that control EMT, such as the TGFβ family, which plays a predominant role in this process. The article covers the deconstruction of cell junctions and polarity, cytoskeletal changes, and the remodeling of the extracellular matrix (ECM) during EMT. Additionally, it explores the role of alternative splicing and microRNAs in regulating gene expression and EMT progression. The authors also review the involvement of tyrosine kinase receptors and growth factors in inducing EMT, emphasizing the roles of PI3K-AKT, ERK MAPK, p38 MAPK, and JNK pathways. Overall, the article provides a detailed and integrated view of the molecular mechanisms underlying EMT, highlighting its significance in various biological and pathological contexts.