Epithelial-mesenchymal transitions (EMT) are critical processes in development and disease, enabling cells to switch between epithelial and mesenchymal states. This review discusses EMT in amniotes, focusing on gastrulation and neural crest formation. During gastrulation, EMT allows cells to internalize and form germ layers, while neural crest cells undergo EMT to migrate and differentiate into various tissues. EMT is also involved in cancer progression, where cancer cells use similar mechanisms to invade tissues. EMT involves the loss of cell-cell adhesion, disruption of apical-basal polarity, and cytoskeletal remodeling, leading to cell migration. Key regulators include Snail, Zeb, and TGF-β signaling pathways. These processes are essential for embryonic development, but their reactivation in adults can lead to diseases like fibrosis and cancer. The neural crest, an evolutionary novelty, plays a crucial role in forming the vertebrate head and is associated with various congenital malformations. In gastrulation, signaling pathways such as Wnt, FGF, and Nodal regulate EMT, leading to the formation of mesoderm and endoderm. Transcription factors like Snail and Eomesodermin are crucial for EMT, while post-transcriptional regulation also plays a role. During neural crest development, EMT is regulated by similar pathways, with Snail2 being essential for delamination and migration. The extracellular matrix and integrins also play roles in EMT. Mutations in genes involved in EMT can lead to congenital defects, highlighting the importance of EMT in development. Understanding EMT mechanisms may lead to therapies for diseases involving EMT, such as cancer and fibrosis. The review emphasizes the complexity of EMT and its dual role in development and disease.Epithelial-mesenchymal transitions (EMT) are critical processes in development and disease, enabling cells to switch between epithelial and mesenchymal states. This review discusses EMT in amniotes, focusing on gastrulation and neural crest formation. During gastrulation, EMT allows cells to internalize and form germ layers, while neural crest cells undergo EMT to migrate and differentiate into various tissues. EMT is also involved in cancer progression, where cancer cells use similar mechanisms to invade tissues. EMT involves the loss of cell-cell adhesion, disruption of apical-basal polarity, and cytoskeletal remodeling, leading to cell migration. Key regulators include Snail, Zeb, and TGF-β signaling pathways. These processes are essential for embryonic development, but their reactivation in adults can lead to diseases like fibrosis and cancer. The neural crest, an evolutionary novelty, plays a crucial role in forming the vertebrate head and is associated with various congenital malformations. In gastrulation, signaling pathways such as Wnt, FGF, and Nodal regulate EMT, leading to the formation of mesoderm and endoderm. Transcription factors like Snail and Eomesodermin are crucial for EMT, while post-transcriptional regulation also plays a role. During neural crest development, EMT is regulated by similar pathways, with Snail2 being essential for delamination and migration. The extracellular matrix and integrins also play roles in EMT. Mutations in genes involved in EMT can lead to congenital defects, highlighting the importance of EMT in development. Understanding EMT mechanisms may lead to therapies for diseases involving EMT, such as cancer and fibrosis. The review emphasizes the complexity of EMT and its dual role in development and disease.