KIF3C encodes a microtubule-based motor protein that translocates membranous organelles within the cytoplasm and plays a role in ciliary function. The protein belongs to the kinesin superfamily and is preferentially expressed in the brain and central nervous system 1. Structurally, KIF3C contains a conserved motor domain typical of kinesins and an unusually long insertion near the microtubule-binding region 12. KIF3C exhibits markedly discordant functions across disease contexts. In glioma, higher KIF3C expression correlates with longer survival and lower-grade tumors, suggesting a tumor-suppressive role 3. Conversely, in gastric cancer, colorectal cancer, lung squamous cell carcinoma, and prostate cancer, elevated KIF3C expression associates with poor prognosis and enhanced proliferation, migration, and chemoresistance 4567. In multiple myeloma, KIF3C amplification via extrachromosomal circular DNA drives proteasome inhibitor resistance 8. The oncogenic mechanism involves PI3K/AKT pathway activation and, in some contexts, epithelial-mesenchymal transition 9. Recently, pathogenic variants in KIF3C combined with ZNF513 mutations were identified in hereditary gingival fibromatosis, where they increase fibroblast proliferation through PI3K/AKT/mTOR signaling 10. These findings position KIF3C as a potential therapeutic target in PI3K/AKT-driven malignancies, though its tissue-dependent role requires careful therapeutic consideration.