KIF3A is a kinesin motor protein essential for primary cilia formation and function. It operates as a microtubule-based anterograde translocator, exhibiting plus end-directed microtubule sliding activity and playing critical roles in centriole cohesion, subdistal appendage organization, and ciliary basal feet formation 1. Beyond structural functions, KIF3A participates in multiple signaling pathways including Sonic Hedgehog signaling, where alternative splicing-mediated KIF3A exon skipping promotes SHH-subgroup medulloblastoma progression through Gli2 activation 2. KIF3A dysfunction associates with multiple diseases. Reduced KIF3A expression, driven by disease-associated SNPs that increase DNA methylation, impairs skin barrier homeostasis and promotes atopic dermatitis development through disrupted junctional proteins and increased transepidermal water loss 3. Kif3a-deficient mice develop transcriptomic profiles closely resembling pediatric atopic dermatitis 4. Additionally, KIF3A polymorphisms show significant associations with childhood asthma and aspirin-intolerant asthma, potentially through impaired mucus and allergen clearance 5 6. In nasopharyngeal carcinoma, KIF3A knockdown reduces tumor stem cell proliferation and invasion by suppressing HIF-1 and NF-κB signaling 7. Cardiac fibroblasts require primary cilia-dependent KIF3A function for transforming growth factor β signaling and fibrogenesis during myocardial injury 1.