NDUFA12 is an accessory subunit of mitochondrial Complex I (NADH:ubiquinone oxidoreductase), essential for electron transfer from NADH to the respiratory chain 1. Unlike core catalytic subunits, NDUFA12 is required for assembly and stability of the electron-transferring Q module in Complex I's peripheral arm, rather than direct catalysis 1. Biallelic loss-of-function NDUFA12 variants cause mitochondrial Complex I deficiency with substantial phenotypic heterogeneity 23. Clinical presentations range from severe Leigh syndrome with basal ganglia abnormalities to isolated optic atrophy, with disease onset and progression varying even among patients carrying identical variants 234. NDUFA12 defects represent an underappreciated cause of inherited optic neuropathies, including autosomal recessive Leber Hereditary Optic Neuropathy 4. Beyond mitochondrial disease, NDUFA12 has emerged as a therapeutic target in cancer biology. The compound Ertredin and its analogue 7MeERT inhibit cancer cell proliferation through NDUFA12 binding, suppressing oxidative phosphorylation and reducing oxygen consumption 56. Additionally, variants near NDUFA12 were associated with age-related executive function decline in females in genome-wide studies 7, and NDUFA12 was identified among obesity-associated genes in adipose tissue expression studies 8.