CDK15 (cyclin-dependent kinase 15) is a serine/threonine protein kinase with dual roles in cell survival and proliferation. As an antiapoptotic protein, CDK15 phosphorylates survivin at threonine-34, conferring resistance to TRAIL-induced apoptosis in cancer cells 1. Beyond apoptosis regulation, CDK15 promotes tumor progression through kinase-dependent mechanisms: in colorectal cancer, CDK15 phosphorylates PAK4 at serine-291, activating β-catenin/c-Myc and MEK/ERK signaling pathways to drive proliferation and anchorage-independent growth 2. CDK15 is significantly upregulated across multiple malignancies. In breast cancer, high CDK15 expression correlates with poor prognosis, advanced TNM staging, lymph node metastasis, and reduced survival 3. Similarly, elevated CDK15 in colorectal cancer negatively associates with patient survival, with CDK15 knockdown suppressing tumor growth in preclinical models 2. In hepatocellular carcinoma, miR-483-5p functions as a tumor suppressor by downregulating CDK15 4. Genomic mechanisms disrupting CDK15 include EBV integration into CDK15 introns, which decreases gene expression in nasopharyngeal carcinomas 5, and HBV-mediated integration generating fusion transcripts 6. A rare CDK15-ALK fusion was identified in lung adenocarcinoma, responding to ALK-targeted therapy 7. These findings establish CDK15 as a functionally relevant oncogene across multiple cancer types, warranting investigation as a therapeutic target.