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Ferroptosis is a new form of programmed cell death characterized by iron-dependent accumulation of lipid reactive oxygen species (ROS). In the process of ferroptosis, excessive iron accumulation can trigger Fenton reaction in cells, induce massive production of ROS, and finally cause lipid peroxidation, DNA damage and protein degradation (Dixon et al., 2012). In the last decade, there has been an increased interest in the process and function of ferroptosis due to its relationship to various diseases including cancer. Following treatment with ferroptosis inducers (e.g., erastin, RSL3 and sorafenib), the anti-tumor response can be achieved in various cancer types and models, highlighting the need for better understanding of molecular mechanism of ferroptosis (Zhao et al., 2020). In this editorial, we provide a platform for most recent advances in the mechanism of ferroptosis initiation and execution in cancer cells, along with the potential clinical application of ferroptosis-related drugs to cancer therapy. The Research Topic represents a collection of 10 original research articles, seven review articles ranging from theory to application. There are three main metabolic pathways in ferroptosis, namely, iron metabolism, lipid metabolism and amino acid metabolism. Among them, the first two metabolism types contribute to increased generation of lipid peroxide, whereas the latter is known to be responsible for antioxidant response. Lipid peroxidation plays an essential part in the mechanism of ferroptosis. Its major process is to convert the polyunsaturated fatty acids (PUFA) to toxic PUFA-PE-OH, leading to initiation of cell death cascades (Conrad et al., 2018). These reactions were successively catalyzed by the acyl-CoA synthetase long-chain family member 4 (ACSL4), polyunsaturated fatty acids-phosphatidylethanolamine (LPCAT3) catalysis and arachidonic acid lipoxygenases (ALOXS). Interestingly, OPEN ACCESS