GLRX5 is a monothiol glutaredoxin that functions as a critical mitochondrial iron-sulfur (Fe/S) cluster transfer protein 1. It receives 2Fe/2S clusters from the scaffold protein ISCU and mediates their transfer to apoproteins, the 4Fe/4S cluster biosynthesis machinery, or export from mitochondria 123. GLRX5 forms a tetrameric complex when bound to [2Fe-2S] clusters through coordination by conserved cysteine residues and glutathione molecules 4. The protein is essential for regulating hemoglobin synthesis through the iron-sulfur protein ACO1 and supporting lipoate-dependent enzyme function 15. Clinically, GLRX5 mutations cause sideroblastic anemia and childhood-onset spastic paraplegia with hyperglycinemia 637. In sideroblastic anemia patients, GLRX5 mutations impair heme biosynthetic enzymes ALAS2 and ferrochelatase activity, leading to oxidative stress and mitochondrial dysfunction 6. Additionally, GLRX5 has emerged as a prognostic marker in bladder cancer, where elevated expression correlates with malignant behavior and poor outcomes 8, and as a potential biomarker in acute kidney injury and suicide attempt risk 910.