CDKN3 encodes a dual-specificity protein phosphatase that plays a central role in cell cycle regulation by dephosphorylating CDK2 at threonine-160 in a cyclin-dependent manner 1. The protein possesses both protein tyrosine and serine/threonine phosphatase activities and associates with multiple cyclin-dependent kinases, suggesting a broader role in regulating the G1/S transition and mitosis. In normal cells, CDKN3 transcript and protein levels fluctuate during the cell cycle, peaking during mitosis 2. CDKN3 is frequently overexpressed across most human cancers and correlates with reduced survival in several tumor types, including gastric cancer, hepatocellular carcinoma, ovarian cancer, and cervical cancer 3456. Mechanistically, CDKN3 overexpression in rapidly dividing tumors appears driven by the increased proportion of mitotic cells rather than genetic alterations 2. The gene affects tumorigenesis primarily through dysregulation of cell cycle checkpoints, mitotic spindle control, and associations with oncogenic pathways including P53 and PI3K-AKT signaling 7. CDKN3 knockdown suppresses cancer cell proliferation and promotes apoptosis 5, positioning the gene as a potential therapeutic target for cancer treatment 6.