SLC25A43 is a mitochondrial ATP transporter located on chromosome X that regulates cellular responses to oxidative stress and cell cycle progression. Functionally, SLC25A43 knockout cells show reduced ROS-induced damage and higher viability under oxidative stress, with activation of mitochondrial protective genes including Nlrx1 1. The protein acts as a mitochondrial checkpoint regulator affecting G1-to-S phase transition, with context-dependent effects: in normal breast epithelial cells, SLC25A43 knockdown inhibits cell cycle progression and proliferation, while in HER2-positive cancer cells it paradoxically increases proliferation 2. SLC25A43 is frequently deleted or epigenetically silenced in multiple cancers. Deletion occurs in 48% of HER2-positive breast cancers, 42% of cervical cancers, and 67% of lung cancers 3, with methylation serving as an alternative inactivation mechanism 4. Expression is significantly reduced in basal cell carcinoma compared to healthy skin 5. SLC25A43 influences drug efficacy, particularly reducing paclitaxel and trastuzumab cytotoxicity in breast cancer cells through altered drug-induced cell cycle arrest 6. Recent evidence suggests potential involvement in mitochondrial glutathione metabolism in cancer contexts 7. Survival analysis identified SLC25A43 as prognostically significant in glioblastoma 8, supporting its broader role in cancer biology.