KIFC3 is a minus-end-directed microtubule motor protein with critical roles in cellular homeostasis and disease pathogenesis. As a C-terminal kinesin family member, KIFC3 functions in microtubule-based transport processes and is abundantly expressed in retina, retinal pigment epithelium, kidney, and lung 1. Mechanistically, KIFC3 mediates several distinct cellular processes. It participates in DNA damage repair by reversing DNA double-strand break-capturing nuclear envelope tubules (dsbNETs) through collaboration with DDR machinery and other kinesins 2. KIFC3 is recruited to polyglutamylated nucleus-to-cilium microtubule arrays (sinc-MTs) and interacts with centrosomal protein CENEXIN1 to facilitate FBF1 translocation to PML-NBs, a prerequisite for senescence induction in mammalian cells 3. Clinically, KIFC3 dysregulation is associated with multiple malignancies. KIFC3 is significantly upregulated in esophageal squamous cell carcinoma, hepatocellular carcinoma, gastric cancer, and non-small cell lung cancer, correlating with poor prognosis [PMID:36051093; 4; 5; 6; 77]. In these cancers, KIFC3 promotes proliferation, migration, and invasion through activation of multiple signaling pathways including β-catenin, PI3K/AKT/mTOR, and Notch1 signaling. These findings position KIFC3 as a potential therapeutic target for cancer treatment.