KIFC2 is a kinesin-14 family motor protein with dual roles in normal neuronal function and cancer progression. In neurons, KIFC2 regulates apical dendrite development by localizing the Scribble scaffold complex to promote cGMP synthesis 1, and likely participates in microtubule-dependent axonal transport 2. However, KIFC2 is significantly amplified and overexpressed across multiple cancers, where it functions as an oncogenic driver. In hormone receptor-positive breast cancer, KIFC2 stabilizes CDK4 protein through enhanced USP9X interaction, promoting tumor growth and conferring resistance to endocrine therapy and CDK4/6 inhibitors 3. In prostate cancer, KIFC2 promotes progression by activating the NF-κB signaling pathway, increasing p65 expression and nuclear translocation 4, while also correlating with enhanced proliferation through KRAS and PI3K-AKT pathway activation 5. Across colon adenocarcinoma, bladder cancer, and other malignancies, elevated KIFC2 expression associates with poor prognosis, increased tumor mutational burden, and reduced anti-tumor immune responses 67. These findings establish KIFC2 as a promising prognostic biomarker and potential therapeutic target across multiple cancer types, despite its essential role in normal neuronal development.