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Tat-Beclin-1 has broader aging relevance because autophagy intersects with multiple hallmarks: Disabled macroautophagy (direct target) Loss of proteostasis (aggregate clearance) Mitochondrial dysfunction (mitophagy -- selective autophagy of damaged mitochondria) Deregulated nutrient sensing (autophagy is regulated by mTOR and AMPK) Cellular senescence (autophagy modulates SASP composition and can influence senescence onset) This broader coverage gives Tat-Beclin-1 a theoretical advantage as a single-agent anti-aging intervention