SLC25A25 is a mitochondrial electroneutral antiporter that mediates calcium-dependent ATP-Mg²⁺/inorganic phosphate exchange across the inner mitochondrial membrane 1. By regulating the mitochondrial adenyl nucleotide pool, it adapts cellular metabolism to changing energetic demands 1. SLC25A25 acts downstream of the ciliary calcium-permeable channel TRPP2, establishing a conserved molecular link between ciliary signaling and mitochondrial metabolism 2. This pathway is essential for left-right patterning and other ciliary-dependent physiological functions 2. Clinically, SLC25A25 dysfunction has disease relevance across multiple conditions. Loss-of-function mutations impair oxidative phosphorylation and increase oxidative stress 1, while a heterozygous dominant variant (p.Gln349His) reducing calcium-regulated ATP transport to ~20% of wild-type activity was identified in families with recurrent kidney stones, likely through impaired ATP provision for renal solute transport 3. The gene is also implicated in cancer biology, with its antisense RNA (SLC25A25-AS1) acting as a tumor suppressor—decreased expression in colorectal cancer promotes proliferation, chemoresistance, and epithelial-mesenchymal transition 4. Additionally, SLC25A25 expression changes in delayed-onset muscle soreness correlate with mitochondrial damage and inflammatory immune responses 5. Exercise acutely upregulates SLC25A25 in endothelial cells, suggesting metabolic adaptation roles 6.