SLC25A10 is a mitochondrial inner membrane transporter that catalyzes electroneutral exchange of dicarboxylates (malate, succinate, malonate), phosphate, and inorganic sulfur-containing anions 1. The protein functions as a monomer using a ping-pong kinetic mechanism, where substrates bind and dissociate consecutively at a single binding site rather than simultaneously 1. SLC25A10 plays critical roles in gluconeogenesis, fatty acid metabolism, urea synthesis, and sulfur metabolism, particularly in hepatic tissues, and regulates adipocyte fatty acid release and systemic insulin sensitivity. In cancer pathophysiology, SLC25A10 is significantly upregulated in colorectal, cervical, and osteosarcoma tissues and correlates with poor prognosis 234. SLC25A10 contributes to oncogenic progression through multiple mechanisms: (1) facilitating succinate export to activate the succinate/SUCNR1 axis on macrophages, promoting M2 polarization of tumor-associated macrophages 2; (2) transporting glutathione into mitochondria to activate the mtGSH/GPX4 axis, suppressing ferroptosis-mediated cell death 35; and (3) promoting mitochondrial function necessary for tumor cell proliferation and migration 6. Protein stability of SLC25A10 is regulated by ubiquitination: STUB1-mediated ubiquitination negatively regulates SLC25A10 6, while INHBA acts as a scaffold protein to inhibit TRIM21-mediated degradation 2. Low SLC25A10 expression associates with poor ovarian cancer survival and chemotherapy resistance 7. These findings establish SLC25A10 as a therapeutic target for cancer treatment.