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Although N-acetylcysteine (NAC) directly influences the pool of extracellular cystine and intracellular cysteine via a series of plasmatic redox reactions, in order to be effective, intracellular cysteine precursors must be designed to enter erythrocytes rapidly and use high activity enzymes within erythrocytes to liberate cysteine (Whillier et al., 2009

C., Hagiwara, A., Han, J., & Lee, J

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Furthermore, Nrf2 overexpression raises the expression levels of FSP1, GPX4, SLC7A11, and other related proteins in lung cancer [114, 115], and obstructs the therapeutic process of ferroptosis activators by shielding lung cancer cells from ferroptosis