The article discusses the relationship between epithelial-to-mesenchymal transition (EMT), cancer stem cells (CSCs), and drug resistance in cancer. It highlights how EMT, a process that transforms epithelial cells into mesenchymal cells, is closely linked to the CSC state, which is characterized by the ability to self-renew and initiate tumors. The EMT program is driven by various signaling pathways, including TGFβ-SMAD, Wnt, and others, and involves the activation of transcription factors such as Snail, ZEB, and TWIST. These factors regulate the expression of genes associated with the mesenchymal phenotype, leading to the loss of epithelial traits and the acquisition of stem-like properties. This connection between EMT and CSCs explains why CSCs are more resistant to conventional therapies and can lead to clinical relapse. The article also discusses the role of the tumor microenvironment, including carcinoma-associated fibroblasts and inflammatory cells, in promoting EMT and CSC formation. Additionally, it explores the mechanisms by which EMT contributes to metastasis, including the ability of EMT-activated cells to form metastatic colonies and the role of EMT in enabling cancer cells to adapt to new environments. The study emphasizes the importance of understanding the EMT-CSC link for developing effective therapies targeting cancer.The article discusses the relationship between epithelial-to-mesenchymal transition (EMT), cancer stem cells (CSCs), and drug resistance in cancer. It highlights how EMT, a process that transforms epithelial cells into mesenchymal cells, is closely linked to the CSC state, which is characterized by the ability to self-renew and initiate tumors. The EMT program is driven by various signaling pathways, including TGFβ-SMAD, Wnt, and others, and involves the activation of transcription factors such as Snail, ZEB, and TWIST. These factors regulate the expression of genes associated with the mesenchymal phenotype, leading to the loss of epithelial traits and the acquisition of stem-like properties. This connection between EMT and CSCs explains why CSCs are more resistant to conventional therapies and can lead to clinical relapse. The article also discusses the role of the tumor microenvironment, including carcinoma-associated fibroblasts and inflammatory cells, in promoting EMT and CSC formation. Additionally, it explores the mechanisms by which EMT contributes to metastasis, including the ability of EMT-activated cells to form metastatic colonies and the role of EMT in enabling cancer cells to adapt to new environments. The study emphasizes the importance of understanding the EMT-CSC link for developing effective therapies targeting cancer.