Programmed cell death (PCD) is a fundamental process in life, crucial for growth, development, aging, and disease. PCD involves the activation and regulation of specific genes, leading to autonomous and orderly cell death. Recent research has revealed multiple PCD pathways, each with unique signaling pathways and morphological characteristics. This article reviews and summarizes these pathways, analyzes their morphological features and biomarkers, and discusses their roles in diagnosing and treating various diseases, particularly malignant tumors. Key points include: 1. Different types of PCD have distinct signaling pathways and morphological characteristics. 2. Understanding the specific biomarkers and regulatory mechanisms of various PCD pathways is vital for targeted treatment. 3. Future research should focus on the molecular mechanisms and cross-links between different PCD types, as well as identifying specific drug targets. The article also provides a detailed classification of PCD types, including apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy-dependent cell death, mitotic catastrophe, immunogenic cell death, entosis, parthanatos, cuproptosis, disulfidptosis, NETosis, lysosome-dependent cell death, alkaliptosis, and oxieptosis. Each type is described in terms of its morphological characteristics, molecular mechanisms, and potential therapeutic applications. Open questions include: 1. How many forms of PCD exist, and how can they be classified scientifically? 2. Which PCD pathways are preferentially activated, and how can different pathways be coordinated for specific diseases? 3. How can the potential off-target effects of PCD induction be effectively prevented and controlled for disease therapy? The article concludes by highlighting the importance of further research to understand the complex mechanisms of PCD and to develop targeted therapies.Programmed cell death (PCD) is a fundamental process in life, crucial for growth, development, aging, and disease. PCD involves the activation and regulation of specific genes, leading to autonomous and orderly cell death. Recent research has revealed multiple PCD pathways, each with unique signaling pathways and morphological characteristics. This article reviews and summarizes these pathways, analyzes their morphological features and biomarkers, and discusses their roles in diagnosing and treating various diseases, particularly malignant tumors. Key points include: 1. Different types of PCD have distinct signaling pathways and morphological characteristics. 2. Understanding the specific biomarkers and regulatory mechanisms of various PCD pathways is vital for targeted treatment. 3. Future research should focus on the molecular mechanisms and cross-links between different PCD types, as well as identifying specific drug targets. The article also provides a detailed classification of PCD types, including apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy-dependent cell death, mitotic catastrophe, immunogenic cell death, entosis, parthanatos, cuproptosis, disulfidptosis, NETosis, lysosome-dependent cell death, alkaliptosis, and oxieptosis. Each type is described in terms of its morphological characteristics, molecular mechanisms, and potential therapeutic applications. Open questions include: 1. How many forms of PCD exist, and how can they be classified scientifically? 2. Which PCD pathways are preferentially activated, and how can different pathways be coordinated for specific diseases? 3. How can the potential off-target effects of PCD induction be effectively prevented and controlled for disease therapy? The article concludes by highlighting the importance of further research to understand the complex mechanisms of PCD and to develop targeted therapies.