Ferroptosis is a form of programmed cell death characterized by iron-dependent lipid peroxidation, leading to prominent features of iron accumulation and lipid peroxidation. It has significant implications in both physiological and pathological contexts, particularly in cancer and other medical conditions. On one hand, ferroptosis exhibits anti-cancer properties by triggering cell death in malignant cells. On the other hand, it can damage normal cells, contributing to the development of various diseases such as cardiovascular disorders and neurodegenerative conditions. The paper reviews the development history, concept, and mechanism of ferroptosis, focusing on methods to induce ferroptosis in tumors and its utilization in different medical conditions. It also emphasizes strategies to inhibit ferroptosis and highlights key contradictions in its control. Potential research avenues in associated domains are suggested. Ferroptosis is a cellular demise mechanism that relies on iron and is triggered by the accumulation of reactive oxygen species (ROS) and lipid peroxidation. It has been shown to inhibit tumor cell proliferation and impede migration and invasion. However, it can also damage normal cells, making its precise targeting crucial. The mechanism of ferroptosis involves the interplay between lipid peroxidation and antioxidant mechanisms, regulated by factors such as iron metabolism and lipid ROS metabolism. Key regulatory proteins include GPX4, which plays a crucial role in maintaining cellular antioxidant capacity. Ferroptosis has been implicated in various diseases, including neurodegenerative disorders like Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). These diseases are characterized by iron accumulation, ROS production, and lipid peroxidation, which contribute to neuronal damage and dysfunction. The paper discusses methods to promote ferroptosis in cancer cells, such as increasing intracellular iron levels, depleting glutathione (GSH), and inhibiting GPX4. It also explores strategies to inhibit ferroptosis, including targeting ferroptosis suppressor proteins and modulating the tumor microenvironment. Ferroptosis is a double-edged sword, offering potential therapeutic benefits in cancer while posing risks in normal cells. Balancing ferroptosis in clinical applications remains a critical challenge.Ferroptosis is a form of programmed cell death characterized by iron-dependent lipid peroxidation, leading to prominent features of iron accumulation and lipid peroxidation. It has significant implications in both physiological and pathological contexts, particularly in cancer and other medical conditions. On one hand, ferroptosis exhibits anti-cancer properties by triggering cell death in malignant cells. On the other hand, it can damage normal cells, contributing to the development of various diseases such as cardiovascular disorders and neurodegenerative conditions. The paper reviews the development history, concept, and mechanism of ferroptosis, focusing on methods to induce ferroptosis in tumors and its utilization in different medical conditions. It also emphasizes strategies to inhibit ferroptosis and highlights key contradictions in its control. Potential research avenues in associated domains are suggested. Ferroptosis is a cellular demise mechanism that relies on iron and is triggered by the accumulation of reactive oxygen species (ROS) and lipid peroxidation. It has been shown to inhibit tumor cell proliferation and impede migration and invasion. However, it can also damage normal cells, making its precise targeting crucial. The mechanism of ferroptosis involves the interplay between lipid peroxidation and antioxidant mechanisms, regulated by factors such as iron metabolism and lipid ROS metabolism. Key regulatory proteins include GPX4, which plays a crucial role in maintaining cellular antioxidant capacity. Ferroptosis has been implicated in various diseases, including neurodegenerative disorders like Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). These diseases are characterized by iron accumulation, ROS production, and lipid peroxidation, which contribute to neuronal damage and dysfunction. The paper discusses methods to promote ferroptosis in cancer cells, such as increasing intracellular iron levels, depleting glutathione (GSH), and inhibiting GPX4. It also explores strategies to inhibit ferroptosis, including targeting ferroptosis suppressor proteins and modulating the tumor microenvironment. Ferroptosis is a double-edged sword, offering potential therapeutic benefits in cancer while posing risks in normal cells. Balancing ferroptosis in clinical applications remains a critical challenge.