SLC25A24 is an electroneutral antiporter mediating adenyl nucleotide transport across the inner mitochondrial membrane 1. It functions as an ATP-magnesium/inorganic phosphate antiporter with broad specificity for adenyl nucleotides, regulating the mitochondrial matrix adenyl nucleotide pool to adapt to cellular energetic demands 1. The protein also demonstrates calcium-buffering capacity through mitochondrial calcium-phosphate precipitate formation, potentially protecting against oxidative stress-induced cell death 1. SLC25A24 plays significant roles in multiple physiological processes. It regulates body fat mass and adipogenesis, as Slc25a24-knockout mice exhibited reduced body weight and white adipose tissue with inhibited adipocyte differentiation 2. In colorectal cancer, SLC25A24 acts as an independent prognostic marker; reduced expression correlates with worse survival, while overexpression suppresses proliferation, migration, and invasion through PKG1-dependent cGMP signaling 3. Notably, SLC25A24 expression increases in microsatellite-instability colorectal cancer showing greater immune checkpoint inhibitor responsiveness 3. SLC25A24 participates in fibroblast recruitment and tumor microenvironment remodeling via CCR5-SLC25A24 signaling in colorectal cancer 4. Clinical relevance includes Fontaine progeroid syndrome association and emerging links to psychiatric conditions. SLC25A24 methylation patterns correlate with callous-unemotional traits in conduct disorder, associating with altered gray matter volume in brain regions implicated in socioemotional processing 5. Recent findings suggest SLC25A24 as a sepsis mortality biomarker 6 and genetic cause of syndromic short stature 7.