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This mechanism achieves the suppression of ELT3 cell proliferation [140]

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This finding suggests that p16INK4A could be involved in regulating melanocyte function in non-segmental vitiligo, possibly as a response to oxidative or inflammatory stressors in the skin microenvironment.32 Trained immunity and immune tolerance A long-term increase in innate memory function, described as trained immunity after vaccination and in other inflammatory diseases, could play a role as an enhancer and continuous trigger in the pathogenesis of vitiligo