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Mao found that treating cancer cells with GPX4 inhibitors resulted in acute depletion of N-carbamyl-L-aspartate (C-ASP, a pyrimidine biosynthesis intermediate), accompanied by accumulation of uridine, which could be inhibited by fer-1, a ferroptosis inhibitor [18]

3g, GS siRNA transfection, which led to more than 60% GS gene silencing, similarly increased the sensitivity of hepatocytes to TNF killing, suggesting that increased GSSG accumulation mechanistically contributed to cellular glutathione imbalance-induced susceptibility to TNF-induced cell death

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