KIFAP3 (kinesin-associated protein 3) is a component of the kinesin II motor complex involved in microtubule-based cellular transport and ciliary function. The protein binds to the tail domain of KIF3A/KIF3B heterodimers to form a functional heterotrimeric complex and regulates its membrane association, facilitating processes including spindle pole organization, chromosome 1, and plus-end-directed vesicle transport 1. In amyotrophic lateral sclerosis (ALS), KIFAP3 variants show complex disease associations. Initial genome-wide analysis identified SNP rs1541160, where the favorable CC genotype correlated with reduced KIFAP3 expression and 14-month survival advantage in sporadic ALS 2. However, this finding demonstrated inconsistent replication across independent cohorts 31. The CC genotype was associated with upper motor neuron-predominant ALS phenotype, suggesting KIFAP3 modifies clinical presentation rather than overall survival universally 4. Beyond ALS, KIFAP3 variants associate with endometriosis and fat distribution through WNT signaling pathways 5. A long noncoding RNA derived from KIFAP3 (KIFAP3-5:1) suppresses epithelial-mesenchymal transition in diabetic nephropathy by targeting PRRX1, with plasma levels correlating with renal dysfunction severity 6. Additionally, KIFAP3 mutations may contribute to basal cell carcinoma development through ciliary dysfunction affecting Hedgehog signaling 7.