NDUFA9 is an accessory subunit of mitochondrial respiratory chain Complex I (NADH:ubiquinone oxidoreductase) that plays a critical structural rather than catalytic role 1. NDUFA9 is essential for stabilizing the junction between the membrane and matrix arms of Complex I, a late assembly step required for proper Complex I biogenesis 1. Loss of functional NDUFA9 results in impaired Complex I assembly, accumulation of membrane arm subcomplexes lacking matrix arm markers, and cell growth defects under oxidative phosphorylation-dependent conditions 1. NDUFA9 mutations cause Mitochondrial Complex I Deficiency, Nuclear Type 26, reflecting its essential role in oxidative metabolism. The gene's expression is dysregulated in several disease contexts: it serves as a diagnostic biomarker in sepsis-induced myocardial dysfunction 2, is targeted by miR-34a-5p in Huntington's disease pathomechanisms 3, and is involved in the LINC01133-hsa-miR-4726-5p-NDUFA9 axis mediating astrocytic dysfunction from HIV and cocaine coexposure 4. NDUFA9 expression is also altered in idiopathic pulmonary fibrosis and pemphigus vulgaris, implicating oxidative phosphorylation dysfunction in these pathologies 56. These findings suggest NDUFA9 represents a convergence point for multiple disease mechanisms involving mitochondrial bioenergetics.