NDUFB9 encodes an accessory subunit of mitochondrial respiratory Complex I that functions in electron transport from NADH to ubiquinone 1. While not directly involved in catalysis, NDUFB9 plays important regulatory roles in mitochondrial function and cellular metabolism. The protein stabilizes PINK1 and promotes mitophagy through the PINK1/Parkin pathway, which is crucial for mitochondrial quality control 2. Loss of NDUFB9 expression has been associated with multiple pathological conditions. In breast cancer, NDUFB9 downregulation promotes cell proliferation, migration, and invasion by elevating mitochondrial reactive oxygen species (mtROS), disturbing NAD+/NADH balance, and depleting mitochondrial DNA, potentially through Akt/mTOR/p70S6K signaling and epithelial-mesenchymal transition 3. NDUFB9 expression is decreased in depression models and its overexpression alleviates depressive behaviors by restoring mitochondrial function and enhancing mitophagy 2. The gene also serves as a diagnostic biomarker for osteoarthritis 4 and shows altered expression in asthma 5. NDUFB9 has been identified as a candidate gene for cocaine dependence through genome-wide association studies 6, and its expression is regulated by DNA methylation in diet-induced obesity 7.