MTARC1 encodes mitochondrial amidoxime-reducing component 1 (mARC1), a molybdenum-dependent oxidoreductase that catalyzes reduction of N-oxygenated compounds including amidoxime prodrugs and N-hydroxylated substrates 12. The enzyme accepts electrons from NADH via cytochrome b5 reductase and cytochrome b5 to cleave N-OH bonds, enhancing drug bioavailability and potentially regulating endogenous nitric oxide biosynthesis 12. Clinically, MTARC1 has emerged as a key modifier of steatotic liver disease pathogenesis. Protective genetic variants in MTARC1 (particularly p.Ala165Thr) are associated with reduced hepatic steatosis, lower liver enzymes, and altered plasma lipid profiles 34. Conversely, increased MTARC1 mRNA associates with fatty liver disease progression 3. Mechanistically, hepatocyte mARC1 knockdown decreases hepatic lipid accumulation, increases triglyceride secretion, and alters lipid metabolism pathways in both cultured hepatocytes and mouse models 35. The protein also modulates lipid homeostasis in adipocytes 5. Importantly, MTARC1 p.Ala165Thr carriers show 39-50% reduced liver-related mortality without increased cardiovascular risk 4, establishing MTARC1 inhibition as a promising therapeutic target for metabolic dysfunction-associated steatotic liver disease 6.