NCAPH is a regulatory subunit of the condensin complex, which catalyzes conversion of interphase chr2 into condensed mitotic chr2 by introducing positive supercoils into DNA in the presence of topoisomerases. Early in neurogenesis, NCAPH plays an essential role in accurate mitotic chromosome 2 in neural stem cells, ultimately affecting neuron pool and cortex size. Beyond its structural roles, NCAPH is frequently overexpressed across multiple solid tumors and drives oncogenic progression through multiple signaling pathways 1. In breast cancer, elevated NCAPH correlates with adverse luminal A tumor progression and poor chemotherapy response, with a 10-gene signature (GSLA10) incorporating NCAPH expression outperforming standard prognostic tools for identifying patients at recurrence risk 2. In cervical cancer, NCAPH promotes cell proliferation by inhibiting autophagy through the AKT/mTOR pathway, and this effect is counteracted by TRIM21-mediated ubiquitination and degradation 3. In lung adenocarcinoma, high NCAPH expression independently predicts poor overall survival and disease-free survival 4. Mechanistically, NCAPH activates oncogenic signaling including β-catenin/PD-L1, PI3K/AKT, and MEK/ERK pathways 1, and interacts with YAP1 to promote breast cancer stemness 5. In head and neck squamous cell carcinoma, NCAPH stabilizes PD-L1 protein and promotes immune evasion; topotecan, a topoisomerase I inhibitor, promotes NCAPH degradation and reverses this effect 6. These findings position NCAPH as a multimodal therapeutic target across cancer types.