The chapter examines whether relocating the 13 protein‑coding genes of human mitochondrial DNA (mtDNA) into the nuclear genome could prevent age‑accelerating mtDNA damage and potentially create extremely long‑lived humans. It outlines the scientific rationale—mtDNA’s high mutation rate and vulnerability—as well as the profound technical barriers, including genetic code incompatibilities, epigenetic regulation, hydrophobic protein import, mito‑nuclear co‑evolution, and complex assembly requirements. Ethical concerns around heritable genome engineering and evolutionary consequences of shifting mitochondrial inheritance to both parents are also explored. While single‑gene relocation experiments (such as ND4 for LHON) show early promise, the chapter concludes that full relocation of all 13 genes remains far beyond current capabilities and is relevant mainly as a speculative framework or as a future therapy for mitochondrial disease.