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However, anti-PD-L1 therapy can control the growth of PD-L1-deficient tumors in wild-type mice, suggesting that targeting PD-L1 on host cells specifically MDSCs, rather than tumor cells, may be critical in enhancing anti-PD-1/PD-L1 therapy efficacy [110]

Moreover, properly harnessing the Nrf2/HO-1 axis while managing its potential pro-ferroptotic risks may help maintain redox balance and curb iron overload, thereby offering an additional strategy to alleviate ferroptosis-driven damage in OA (202)

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