KIF13B is a kinesin motor protein that functions as a multitasking regulator of cellular transport and metabolism with broad disease relevance. Primary mechanistically, KIF13B operates as a microtubule-based motor protein involved in intracellular vesicle trafficking and cytoskeletal reorganization 1. It regulates axon formation and undergoes bidirectional intraciliary movement in primary cilia 1, while also interacting with ARF6 signaling pathway components through centaurin-alpha1 binding 2. Beyond transport functions, KIF13B plays critical roles in metabolic homeostasis. In hepatocytes, KIF13B interacts with AMPKα1 to regulate mitochondrial function and suppress sterol regulatory element-binding protein 1-mediated lipogenesis, protecting against metabolic dysfunction-associated fatty liver disease (MAFLD) 3. In macrophages, KIF13B prevents atherosclerosis by maintaining MERTK-mediated efferocytosis through the KIF13B/ITCH/CBL/MERTK axis 4, and suppresses liver inflammation via the STT3A/CTSD/THBS1 axis 5. KIF13B also stabilizes lipid-droplet-associated perilipin 5 (PLIN5) to protect cardiac function during sepsis 6, and collaborates with the nuclear envelope in DNA damage response through DSB-capturing nuclear envelope tubules 7. In abdominal aortic aneurysm, KIF13B stabilizes transcription factor EB through USP9X interaction to maintain macrophage homeostasis 8. Collectively, KIF13B emerges as a potential therapeutic target for metabolic, cardiovascular, and inflammatory diseases.