Previous studies have reported that mtDNA mutations, which partially inactivated ETC complex I and subsequently led to the elevation of mitochondrial reactive oxygen species (mtROS) and nonlethal reduction of NAD+ levels promoted tumor metastasis.[15, 18] Given that mutation of NDUFB9 can lead to complex I deficiency, [13] we investigated mtROS production, NAD+/NADH levels, and mtDNA content in NDUFB9 knockdown and control cells. The gene discussed is NDUFB9; the disease is neoplasm.