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CDK1 directly binds and phosphorylates the S447 site of ACSL4, promoting the ubiquitination degradation of ACSL4, while genetic and pharmacological blocking of CDK1 enhances ACSL4 activity, promoting ferroptosis of colon cancer cells and increasing their susceptibility to oxaliplatin

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As we continue to unravel the complexities of how skin metabolism interacts with T-cell immune responses and inflammatory metabolic pathways, focusing therapeutic efforts on specific subsets of T cells in psoriasis, especially Th17 cells, may pave the way for more personalized medical interventions