CDC25A is a tyrosine protein phosphatase that functions as a dosage-dependent inducer of mitotic progression, primarily through dephosphorylation of cyclin-dependent kinases (CDKs). The enzyme directly dephosphorylates CDK1 to stimulate its kinase activity and dephosphorylates CDK2 in complex with cyclin-E, thereby regulating cell cycle transitions 1. Structurally, CDC25A contains a C-terminal helix critical for binding CDK2-cyclin A complexes, with sequence conservation suggesting it preferentially targets CDK1/2-cyclin A, CDK1-cyclin B, and CDK2/3-cyclin E complexes 1. Clinically, CDC25A functions as an oncogene rather than a tumor suppressor 2. Elevated CDC25A expression correlates with poor prognosis across multiple malignancies. In hepatocellular carcinoma, CDC25A upregulation associates with advanced clinical stage, vascular invasion, and metastasis 3. Similarly, in melanoma, CDC25A inhibition suppresses proliferation and sensitizes cells to chemotherapy and immunotherapy 4. Beyond cancer, CDC25A overexpression drives centrosomal abnormalities in polycystic liver disease, with depletion reducing cyst growth both in vitro and in vivo 5. CDC25A expression also correlates with poor differentiation and tumor invasion in retinoblastoma 6. Recent evidence indicates m6A-mediated stabilization of CDC25A promotes esophagogastric junction adenocarcinoma progression through G1-S acceleration 7, establishing CDC25A as a therapeutic target across multiple tumor types.