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Such as psoriasis, an inflammatory skin disease, is characterized by erythematous plaques resulting from keratinocyte hyperproliferation (95), although the epigenetic elements of trained immunity in human psoriasis have not been fully defined, studies using imiquimod (IMQ)-induced murine psoriasis models have demonstrated that EpSCs retain innate immune memory by maintaining chromatin accessibility following inflammation

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Agents that inhibit the cystine uptake via the cystine/glutamate antiporter (system x c - ) (e.g., sulfasalazine) or directly deplete the GSH from plasma (e.g., cyst(e)inase) triggers ferroptosis and arrests tumorigenesis [224, 225]