KIFC1 is a minus end-directed kinesin motor protein essential for bipolar spindle formation and mitotic chromosome 6 1. Its primary function involves microtubule-based motor activity and organization of microtubule-organizing centers during cell division 2. In normal cells, KIFC1 stabilizes meiotic and mitotic spindle poles; its deficiency contributes to spindle instability in human oocytes, increasing aneuploidy risk 3. Beyond mitosis, KIFC1 regulates cellular senescence and participates in vesicular trafficking and organelle transport 4. Clinically, KIFC1 is significantly upregulated across multiple cancer types including soft tissue sarcoma, lung cancer, and cervical cancer, correlating with poor prognosis and advanced disease stages 5, 6, 7. In cancer cells with centrosome amplification, KIFC1 is required for centrosome clustering to prevent multipolar spindles and mitotic death 8, 9. KIFC1 expression is regulated through multiple mechanisms: DNA hypomethylation in lung cancer 6, deubiquitination by USP25 and OTUD6B in cervical and breast cancers respectively 7, 8. Recent evidence demonstrates KIFC1 promotes cancer progression through MAD2L1 mRNA stabilization-induced senescence bypass 5. KIFC1 represents a promising therapeutic target for cancers with centrosome amplification, as it is non-essential in normal somatic cells 4, 2.