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The researchers constructed a model that introduced the ALAS2 missense mutation erythroblasts derived from human cord blood, in which enhanced BACH1 expression was emerged, leading to increased susceptibility to ferroptosis (Ono et al., 2022)

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Inhibition of cysteine-glutamate transporter protein system (e.g., Erastin) will deplete intracellular GSH, eventually resulting in the inactivation of GPx4 and the accumulation of lipid peroxidation, which can induce cell ferroptosis to a certain extent [75]