Terbinafine, a widely-used antifungal medication, and miglustat, a rare disease treatment, both extended lifespan in C. elegans by activating mitochondrial stress responses. The compounds triggered the mitochondrial unfolded protein response through ATFS-1 while simultaneously engaging insulin/IGF-1 signaling pathways, creating a coordinated cellular stress response involving both ATFS-1 and FOXO transcription factors. This dual-pathway activation represents a departure from typical hormesis mechanisms and suggests sophisticated cross-talk between mitochondrial and metabolic signaling networks. The finding gains practical significance because terbinafine is already FDA-approved and commonly prescribed for fungal infections, potentially offering an immediate repurposing opportunity. However, the translation from worms to humans remains uncertain, though initial experiments in human HEK293T cells showed similar mitochondrial effects. The research contributes to growing evidence that controlled mitochondrial stress - rather than simply protecting mitochondria - may be key to longevity interventions. This approach aligns with hormesis theory but introduces complexity through multi-pathway coordination that could inform more sophisticated anti-aging strategies beyond single-target interventions.