The p62 protein creates liquid-like condensates that actively cluster damaged mitochondria, functioning as a cellular quality control mechanism previously unknown to researchers. This condensation process appears to be a critical step in mitophagy, where cells eliminate dysfunctional mitochondria that could otherwise contribute to cellular aging and metabolic dysfunction. The finding reveals a sophisticated cellular organizing principle where p62 acts as both a molecular scaffold and a sorting mechanism, concentrating damaged organelles for efficient removal. This discovery significantly advances understanding of how cells maintain mitochondrial health throughout aging. The mechanism could explain why mitochondrial quality control deteriorates with age—if p62 condensation becomes less efficient, damaged mitochondria may persist longer, accumulating cellular stress. The research provides a new therapeutic target for age-related diseases linked to mitochondrial dysfunction, including neurodegeneration and metabolic disorders. While the study demonstrates the condensation mechanism, translating this knowledge into interventions requires understanding what regulates p62 condensate formation and whether enhancing this process could extend healthspan. The work represents a paradigm shift from viewing cellular cleanup as random to recognizing it as a precisely orchestrated molecular process.