OLA1 (Obg-like ATPase 1) is an ATP and GTP hydrolyzing enzyme that functions as a critical regulator of cellular metabolism and stress response. Primary function: OLA1 hydrolyzes ATP efficiently and GTP with lower efficiency, serving as a metabolic checkpoint enzyme 1. Mechanism: OLA1 operates through phosphorylation-dependent nuclear translocation, where Ser232/Tyr236 phosphorylation triggers cytoplasmic-to-nuclear translocation, while Thr325 phosphorylation converts its biochemical function from ATPase to GTPase activity, promoting mitochondrial bioenergetic gene expression 1. OLA1 interacts with BRCA1/BARD1 complexes to regulate centrosome function during the cell cycle 2. Additionally, OLA1 is stabilized by the m6A reader IMP2 through ZFAS1, enhancing ATP hydrolysis and glycolytic metabolism 3. Disease relevance: OLA1 dysregulation associates with multiple malignancies—elevated OLA1 expression correlates with poor hepatocellular carcinoma prognosis and enhanced chemotherapy resistance 4, while OLA1 is identified as a glycolysis-related biomarker in gastric cancer 5. OLA1 mutations (Tyr254Cys) and downregulation appear in dilated cardiomyopathy patients 6, 7. Clinical significance: OLA1 serves as a promising independent prognostic predictor for HCC survival and potential therapeutic target. OLA1 knockout mice demonstrate mitochondrial dysfunction with reduced ATP and elevated lactate levels 1, highlighting its therapeutic relevance in metabolic diseases and cancer.