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Furthermore, mitochondrial oxidative stress has been demonstrated to induce ferroptosis via the NRF2-ARE pathway, thereby emphasizing the multifaceted role of ROS in disease mechanisms

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Common ideas include that ferroptotic stress inducing TAMs to repolarize from M2 type to M1 type [128, 208,209,210], inducing ferroptosis of Tregs to reduce negative immune effect [127], targeting system Xc- to alleviate cystine deprivation in TME mediated by myeloid-derived suppressor cells (MDSCs) to promote T cell survival [211] and so on