SLC25A37 (mitoferrin-1) is a mitochondrial iron transporter essential for erythroid development and iron homeostasis. It mediates ferrous iron uptake across the inner mitochondrial membrane, playing a critical role in heme biosynthesis and hemoglobin production 1. The protein functions as part of a paralogous pair with SLC25A28 (mitoferrin-2), and their combined activity is necessary for maintaining mitochondrial iron-sulfur cluster proteins and supporting mitochondrial respiration 1. Beyond hematologic function, SLC25A37 has emerged as a disease-associated gene in multiple pathological contexts. Genome-wide association studies identified SLC25A37 as a major depressive disorder risk gene, with reduced expression in the hippocampus and blood of MDD patients 2. Additionally, SLC25A37 was identified among nine hub mitochondrial genes dysregulated in osteoarthritis, primarily associated with macrophage involvement in disease pathology 3, and was validated as a core gene in neutrophil extracellular trap-related pathways in OA progression 4. Recent genome-wide association studies also linked SLC25A37 variants to cardiac age acceleration 5. Clinically, SLC25A37 represents a potential therapeutic target. In chromosome 8-deleted cancers, SLC25A37 expression status determines vulnerability to its paralog SLC25A28 inhibition, suggesting therapeutic potential through synthetic lethal interactions 1. Furthermore, PINK1-deficient colon tumors with elevated SLC25A37 expression showed sensitivity to iron chelators targeting mitochondrial iron levels 6.