STOX1 is a winged-helix transcription factor located on chromosome 10.1 that regulates cell cycle progression and mitochondrial homeostasis. Primary function: STOX1 binds to the CCNB1 promoter to upregulate cyclin B1 expression, promoting G2/M transition and mitotic entry 1, and induces tau phosphorylation 2. Two major isoforms (STOX1A and STOX1B) compete functionally, with STOX1A serving as the transcriptionally active form 3. Mechanism: STOX1 overexpression disrupts cellular homeostasis through multiple pathways. It impairs hypoxia response, dysregulates antioxidant systems, and creates nitroso-redox imbalance by shifting the free radical balance from ROS toward RNS, leading to peroxynitrite formation and protein nitration 4. STOX1 also alters mitochondrial mass and increases mitochondrial activity, elevating free radical production 4. Disease relevance: STOX1 variants and overexpression are directly associated with preeclampsia pathogenesis, particularly the placental form with growth restriction, involving defective spiral artery remodeling and trophoblast dysfunction 56. Recently, STOX1-A upregulation was identified in hepatocellular carcinoma, promoting proliferation via cyclin B1 upregulation and ROS-mediated PTEN/AKT1 pathway activation 7. Clinical significance: STOX1 emerges as a putative therapeutic target; therapies could modulate isoform ratios, alter subcellular localization, or target downstream pathways in preeclampsia and HCC 3.