CENPF encodes a ~400 kDa kinetochore protein essential for chromosome 1 during mitosis. The protein localizes to kinetochores at late G2 phase and remains associated through metaphase, then relocates to the spindle midzone during anaphase 1. CENPF is required for proper kinetochore function and facilitates the localization of dynein and related transport regulators. Beyond mitosis, CENPF regulates plasma membrane recycling by linking recycling vesicles to the microtubule network, and interacts with RB proteins to modulate cell cycle progression and differentiation. Clinical relevance spans multiple cancer types and developmental disorders. In gastric cancer, elevated CENPF expression—mediated by N6-methyladenosine modification of its mRNA—promotes metastasis and angiogenesis through the FAK/MAPK signaling pathway, correlating with poor overall survival 2. In triple-negative breast cancer, CENPF expression significantly associates with reduced overall survival 3. CENPF has also emerged as a therapeutic target in malignant peripheral nerve sheath tumors; disrupting CENPF expression inhibited growth in both human cell lines and murine models 4. In early-stage lung adenocarcinoma, CENPF was identified as a prognostic biomarker, and the small molecule Aminopurvalanol A showed therapeutic potential against CENPF-expressing tumors 5. Beyond cancer, pathogenic CENPF mutations cause ciliopathy and primary microcephaly, reflecting a novel role in centriolar organization and ciliogenesis 6.