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In addition to the consensus on the prominent role of cystine starvation in blocking GSH synthesis, the present two studies demonstrated two previously under-appreciated metabolic effects that contribute to the ferroptosis-susceptible state in cancer cells under cystine deprivation conditions: loss of GPX4 protein translation and accumulation of oxidative stress-inducing intracellular glutamate (Fig

In addition, sustained JNK activation was amplifies mitochondrial ROS and forms a self-sustaining activation loop (Win et al., 2016)