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In turn, sleep deprivation leads to an upregulation of proapoptotic and proinflammatory markers such as the apoptotic chromatin condensation inducer 1 (Acin1), heat shock protein family E member 1 (HSPE1), and golgin subfamily A member 3 (GOLGA3), thus indicating an overall beneficial function of sleep for myelins maintenance and turnover (Vivo and Bellesi, 2019)