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These biomolecular condensates can modulate biochemical processes, including protein aggregation. Notably, they have been reported to both accelerate and inhibit protein aggregation. Since protein aggregation is often associated with pathological conditions like neurodegenerative diseases, it is crucial to understand the molecular mechanisms underlying the interplay between phase separation and fibril formation. In this review, we discuss how, contrary to intuition, aggregation within the bulk of condensates can be inhibited rather than promoted, even in the presence of elevated local protein concentration. 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