KIF3B is a molecular motor protein that functions as the β-subunit of the heterotrimeric kinesin-2 complex (KIF3A/KIF3B/KAP3), which uses ATP hydrolysis to transport intracellular cargos along microtubules 1. Primary functions include intraflagellar transport essential for cilia assembly and maintenance 2, photoreceptor integrity and opsin trafficking in rod cells 2, and dendritic transport of NMDA receptor complexes 3. KIF3B also plays roles in mitotic spindle assembly and cytokinesis 4. The kinesin-2 complex activity is regulated by a conserved β-hairpin motif in the tail domain that sequesters motor domains from microtubules until cargo adaptors engage 5. Dysfunction of KIF3B causes multiple disease phenotypes. Mutations impair ciliary assembly and cause autosomal-dominant retinitis pigmentosa with associated hepatic fibrosis and polydactyly 2. KIF3B variants reduce NMDA receptor trafficking, disrupting synaptic plasticity and causing schizophrenia-like behavioral defects in mice, with mutations identified in schizophrenia patients 3. Loss-of-function variants cause male infertility through defects in sperm morphology and motility via impaired intraflagellar transport 6. Additionally, elevated KIF3B expression promotes oral squamous cell carcinoma development through increased cell proliferation and migration 7. These diverse disease associations reflect KIF3B's essential role in transport-dependent cellular processes.