SLC25A6 encodes the mitochondrial ADP/ATP antiporter, a membrane protein that catalyzes bidirectional transport of adenine nucleotides across the inner mitochondrial membrane. It mediates ADP influx into the mitochondrial matrix to support ATP synthesis and exports ATP to the cytoplasm to fuel cellular energy demands. Beyond nucleotide transport, SLC25A6 functions as a proton transporter that mediates mitochondrial uncoupling and thermogenesis, with these activities regulated in a reciprocal manner to maintain metabolic homeostasis. The protein also plays a role in mitochondrial permeability transition pore (mPTP) activity; dysfunction or degradation of SLC25A6 alters mPTP opening dynamics and influences apoptotic signaling. Disease associations reflect this multifaceted role in energy metabolism and cell death. In ovarian cancer, MRPL13-mediated SLC25A6 degradation suppresses mPTP opening and promotes tumor progression by enhancing mitochondrial function 1. SLC25A6 dosage affects cardiac electrophysiology: a significant negative correlation exists between SLC25A6 expression level and corrected QT interval duration in sex chromosome X|Y, with pharmacological KATP channel modulation reversing dosage effects 2. In endometriosis and recurrent implantation failure, SLC25A6 emerges as a hub diagnostic biomarker linked to altered endometrial receptivity 3. SLC25A6 expression is altered in spermatozoa from patients with repetitive fertilization failure after ICSI, suggesting paternal mitochondrial dysfunction 4. Recent evidence indicates that carvacrol upregulates SLC25A6 expression through VDAC1 inhibition, improving mitochondrial function and reducing inflammatory injury in endothelial cells 5. The gene represents both a mitochondrial metabolic hub and a potential therapeutic target across cancer, cardiovascular, and reproductive disorders.