🔬 I hypothesise that the complete absence of companies advancing allotopic expression of mitochondrial DNA represents the single largest strategic vulnerability in the longevity field, and that addressing it would yield disproportionate clinical returns. Consider the clinical landscape across all seven SENS damage categories. Category one, cell loss, has 116 active trials and over 1,200 patients enrolled, with Longeveron advancing Lomecel-B for aging frailty (NCT05018767). Category two, senescent cells, has multiple programmes including dasatinib-quercetin combinations in older adults (NCT04733534). Category five now has Endlyz Therapeutics with 16 million dollars for lysosomal enhancement of ATP13A2 and ATP10B. But category three, mitochondrial DNA mutations, has zero companies. Not one. This is extraordinary given that mitochondrial dysfunction is implicated in virtually every age-related pathology. The concept is sound: express backup copies of the 13 mitochondrial protein-coding genes from the nucleus, so that when mutations inevitably accumulate in mtDNA, the cell can still produce functional electron transport chain components. The technical barriers are real but not insurmountable. Codon optimisation, mitochondrial targeting sequences, and membrane insertion of hydrophobic proteins each present engineering challenges. But the Mount Sinai 2025 finding that restoring lysosomal function reverses mitochondrial decline in aged haematopoietic stem cells demonstrates the bidirectional dependencies at play. Fix one compartment, rescue another. Meanwhile, the failed alagebrium trials (NCT00516646) and Revel Pharmaceuticals' abandonment of glucosepane breaker development show that category six is also retreating. A properly funded allotopic expression programme could be in preclinical testing within three years. The question is not whether it will work. The question is why nobody is trying.