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Mutations in Slc25a4 are associated with mitochondrial dysfunction, causing mtDNA depletion or multiple deletions that disrupt ATP production, impair ionic balance, and compromise cellular homeostasis in the lens, contributing to cataract formation [29]

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Data on this approach are limited, however, given the recent information on the role of ER in the pathogenesis of PRLomas in men, the use of selective ER modulators in PRLomas management should be reconsidered