KIF18B (kinesin family member 18B) is a kinesin-8 superfamily member that functions as a key regulator of microtubule dynamics during cell division. In complex with MCAK (KIF2C), KIF18B constitutes the major microtubule plus-end depolymerizing activity in mitotic cells 1. During interphase, KIF18B localizes predominantly to the nucleus, but upon mitotic entry, it binds to astral microtubule plus ends through interaction with EB1 1. KIF18B expression is tightly regulated in a cell cycle-dependent manner, with elevated levels from late G2 through metaphase 2. Aurora kinases negatively regulate the KIF18B-MCAK interaction through phosphorylation, thereby controlling spindle microtubule stability 1. Clinically, KIF18B is widely upregulated across multiple cancer types and functions as an oncogene. High KIF18B expression correlates with poor prognosis, advanced disease stage, and reduced overall survival in gastric cancer, nasopharyngeal carcinoma, lung adenocarcinoma, osteosarcoma, and breast cancer 34567. KIF18B promotes cancer progression through multiple mechanisms: activating Wnt/β-catenin signaling via the Akt/GSK-3β axis, promoting epithelial-mesenchymal transition, and enabling immune evasion through recruitment of regulatory T cells 674. KIF18B overexpression reduces chemotherapy sensitivity, while KIF18B inhibition enhances chemotherapeutic efficacy 3. These findings establish KIF18B as a promising prognostic biomarker and potential therapeutic target across multiple malignancies.