Ferroptosis is a form of programmed cell death driven by iron-dependent lipid peroxidation, characterized by iron accumulation and lipid peroxidation. It plays a dual role in health and disease, with potential anti-cancer properties by inducing ferroptosis in malignant cells, while also damaging normal cells and contributing to diseases like cardiovascular disorders and neurodegenerative conditions. This review explores the paradoxical regulation of ferroptosis in tumors and other diseases, covering its mechanisms, methods of induction, therapeutic applications, and strategies to inhibit it. Ferroptosis is regulated by factors such as glutathione (GSH) levels and the activity of glutathione peroxidase 4 (GPX4). The Fenton reaction generates free radicals that promote lipid peroxidation, leading to cell death. Ferroptosis has shown promise in cancer therapy, with compounds like erastin and sulfasalazine inducing ferroptosis in tumor cells. However, it also contributes to diseases like Alzheimer's and Parkinson's, where iron accumulation and oxidative stress play a role. Research is ongoing to develop strategies to harness ferroptosis for cancer treatment while minimizing harm to normal cells. Nanotechnology is being explored to deliver ferroptosis inducers to tumors, enhancing therapeutic effects. Additionally, understanding the role of ferroptosis in the tumor microenvironment and its interaction with immune cells is crucial for developing effective treatments. Ferroptosis is also implicated in neurodegenerative diseases, where iron dysregulation and oxidative stress contribute to neuronal damage. Overall, ferroptosis represents a complex and dual-edged process with significant implications for both cancer and other diseases.Ferroptosis is a form of programmed cell death driven by iron-dependent lipid peroxidation, characterized by iron accumulation and lipid peroxidation. It plays a dual role in health and disease, with potential anti-cancer properties by inducing ferroptosis in malignant cells, while also damaging normal cells and contributing to diseases like cardiovascular disorders and neurodegenerative conditions. This review explores the paradoxical regulation of ferroptosis in tumors and other diseases, covering its mechanisms, methods of induction, therapeutic applications, and strategies to inhibit it. Ferroptosis is regulated by factors such as glutathione (GSH) levels and the activity of glutathione peroxidase 4 (GPX4). The Fenton reaction generates free radicals that promote lipid peroxidation, leading to cell death. Ferroptosis has shown promise in cancer therapy, with compounds like erastin and sulfasalazine inducing ferroptosis in tumor cells. However, it also contributes to diseases like Alzheimer's and Parkinson's, where iron accumulation and oxidative stress play a role. Research is ongoing to develop strategies to harness ferroptosis for cancer treatment while minimizing harm to normal cells. Nanotechnology is being explored to deliver ferroptosis inducers to tumors, enhancing therapeutic effects. Additionally, understanding the role of ferroptosis in the tumor microenvironment and its interaction with immune cells is crucial for developing effective treatments. Ferroptosis is also implicated in neurodegenerative diseases, where iron dysregulation and oxidative stress contribute to neuronal damage. Overall, ferroptosis represents a complex and dual-edged process with significant implications for both cancer and other diseases.