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The upstream molecular of ACSL4, cyclin-dependent kinase 1 (CDK1) can mediate ubiquitin-mediated degradation of ACSL4 via phosphorylating ACSL4 and recruiting ubiquitin ligase E3 component N-recognition protein 5 (UBR5), ultimately causing ferroptosis and chemotherapy resistance in CRC [138]

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These side effects are usually temporary and improve over time