KIF23 is a kinesin motor protein and essential component of the centralspindlin complex that mediates cytokinesis through microtubule-dependent mechanisms 1. During mitosis, KIF23 functions as a plus-end-directed motor enzyme that positions antiparallel microtubules and facilitates myosin contractile ring formation in a Rho-dependent manner, while also regulating mitotic spindle orientation and apical surface structure in neural stem cells 2. KIF23 activity is regulated by phosphorylation through Aurora B kinase and counteracted by PP1β-MYPT1 phosphatase, which fine-tunes cytokinesis progression 1. KIF23 dysregulation contributes to multiple malignancies. In hepatocellular carcinoma, the miR-107/KIF23 axis controls tumor cell proliferation and survival; elevated KIF23 expression correlates with poor prognosis, and therapeutic targeting via miR-107 overexpression or KIF23 silencing suppresses tumor development 3. Similarly, in colorectal cancer, NAT10-mediated stabilization of KIF23 mRNA activates Wnt/β-catenin signaling to promote progression 4. In lung adenocarcinoma, KIF23 promotes cell proliferation, migration, and invasion 5. Additionally, mutations in KIF23 cause congenital microcephaly through impaired cytokinesis and neural stem cell maintenance 2. These findings establish KIF23 as both a critical regulator of cell division and an emerging therapeutic target across cancer types.