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Stockwell laboratory in 2012, represents an iron-dependent, non-apoptotic cell death modality distinguished by intracellular iron accumulation and lipid peroxidation, culminating in cell membrane disruption and cellular demise ( Disrupted iron homeostasis constitutes a primary trigger for ferroptosis initiation

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Homocysteine is elevated by deficiency of folate and vitamin B 12 because they are required to convert homocysteine back to methionine [25] and high homocysteine may increase DNA damage by impairing FA/BRCA1 required for repair of DNA damage [26]