KIF5B is a microtubule-dependent motor protein with diverse cellular functions. Its primary role involves anterograde axonal and dendritic transport, particularly of mitochondria and lysosomes 12. KIF5B mechanistically functions as a kinesin motor that interacts with adaptor proteins including TRAK1, OPTN, and EndoA2 to facilitate cargo movement along microtubules toward the plus end 23. Additionally, KIF5B regulates DNA damage response by generating DSB-capturing nuclear envelope tubules that enhance DNA repair through microtubule-dependent repositioning mechanisms 4. During immune responses, KIF5B drives polarization of cytolytic granules and microtubule-organizing centers toward immune synapses in NK cells [UniProt annotation]. Disease relevance is substantial: KIF5B fusions with RET and ALK occur in non-small cell lung cancer (~2.5-73% of cases) and ALK-positive histiocytosis respectively, with KIF5B-ALK fusions showing robust responses to ALK inhibition 56. Clinically, KIF5B mutations and dysregulation are implicated in neurodegeneration when associated with impaired mitochondrial transport in amyotrophic lateral sclerosis and normal tension glaucoma contexts 2. Furthermore, KIF5B participates in mechanosensory signal transmission through Piezo2 trafficking in sensory neurons, suggesting therapeutic relevance for pain management 3.