Ferroptosis is a distinct form of programmed cell death characterized by iron accumulation and lipid peroxidation. It differs from classical programmed cell death in morphology and biochemistry, and is linked to various diseases, including cancer and inflammation. Dysfunctional ferroptosis activation is closely associated with the onset of these diseases, making it a promising target for therapeutic intervention. This review explores the regulatory mechanisms of ferroptosis, its impact on cancer and inflammation, and the potential of ferroptosis inducers in overcoming drug-resistant cancers. Ferroptosis is regulated by iron metabolism, lipid metabolism, and amino acid metabolism. Iron accumulation and lipid peroxidation are key drivers of ferroptosis, while glutathione peroxidase 4 (GPX4) plays a crucial role in preventing it. Ferroptosis is involved in tumor suppression and immune functions, with various tumor suppressors, such as p53 and BAP1, regulating ferroptosis. Ferroptosis can also contribute to inflammation by producing inflammatory mediators. The regulation of ferroptosis is influenced by various signaling pathways, including those involving NRF2, HIF, and EMT. Targeting ferroptosis offers new therapeutic opportunities for cancer and inflammatory diseases. Ferroptosis inducers, such as erastin, RSL3, and FIN56, have shown promise in cancer therapy. Additionally, nanoparticle-based ferroptosis inducers are being explored for their potential in cancer treatment. Overall, ferroptosis represents a promising avenue for the treatment of cancer and inflammatory diseases.Ferroptosis is a distinct form of programmed cell death characterized by iron accumulation and lipid peroxidation. It differs from classical programmed cell death in morphology and biochemistry, and is linked to various diseases, including cancer and inflammation. Dysfunctional ferroptosis activation is closely associated with the onset of these diseases, making it a promising target for therapeutic intervention. This review explores the regulatory mechanisms of ferroptosis, its impact on cancer and inflammation, and the potential of ferroptosis inducers in overcoming drug-resistant cancers. Ferroptosis is regulated by iron metabolism, lipid metabolism, and amino acid metabolism. Iron accumulation and lipid peroxidation are key drivers of ferroptosis, while glutathione peroxidase 4 (GPX4) plays a crucial role in preventing it. Ferroptosis is involved in tumor suppression and immune functions, with various tumor suppressors, such as p53 and BAP1, regulating ferroptosis. Ferroptosis can also contribute to inflammation by producing inflammatory mediators. The regulation of ferroptosis is influenced by various signaling pathways, including those involving NRF2, HIF, and EMT. Targeting ferroptosis offers new therapeutic opportunities for cancer and inflammatory diseases. Ferroptosis inducers, such as erastin, RSL3, and FIN56, have shown promise in cancer therapy. Additionally, nanoparticle-based ferroptosis inducers are being explored for their potential in cancer treatment. Overall, ferroptosis represents a promising avenue for the treatment of cancer and inflammatory diseases.