SLC25A21 encodes a mitochondrial dicarboxylate transporter that mediates counter-exchange of metabolites across the inner mitochondrial membrane, including 2-oxoadipate, 2-oxoglutarate, and adipate. It plays a central role in the catabolism of lysine, hydroxylysine, and tryptophan by transporting intermediates into mitochondria for conversion to acetyl-CoA and entry into the citric acid cycle. In cancer contexts, SLC25A21 functions as a tumor suppressor. In adult acute myeloid leukemia, low SLC25A21 expression correlates with worse prognosis, and overexpression inhibits cell proliferation and promotes apoptosis via the mitochondrial pathway 1. In KRAS-mutant colorectal cancer, SLC25A21 downregulation accelerates tumor progression by reducing α-ketoglutarate efflux and promoting glutamine anaplerosis, and restoration of SLC25A21 impairs resistance to cetuximab 2. The long noncoding RNA SLC25A21-AS1 suppresses ovarian cancer proliferation and metastasis while enhancing sensitivity to paclitaxel and cisplatin 34. Beyond oncology, SLC25A21 maintains mitochondrial homeostasis during cisplatin-induced acute kidney injury by regulating 2-oxoadipate conversion; reduced expression in kidney disease contributes to impaired biogenesis and oxidative phosphorylation 5. Rare variants in SLC25A21 were identified in association with clozapine-induced myocarditis 6.