NCAPD2 is a regulatory subunit of the condensin I complex essential for mitotic chromosome 12 and segregation during cell division. Beyond its canonical role in chromosome 12, NCAPD2 has emerged as a significant oncogene across multiple cancer types. In colorectal cancer, NCAPD2 inhibits autophagy through the Ca2+/CAMKK/AMPK/mTORC1 pathway and PARP-1/SIRT1 axis, promoting tumor development 1. In liver cancer, NCAPD2 enhances tumorigenesis via the PI3K-Akt-mTOR signaling pathway, promoting cell proliferation, invasion, and cell cycle progression while inhibiting apoptosis 2. Similarly, in lung adenocarcinoma, NCAPD2 promotes tumor progression through an AKT/MDM2/E2F1 positive feedback loop, where it activates the PI3K/Akt pathway and facilitates MDM2-E2F1 interactions, while E2F1 reciprocally enhances NCAPD2 transcription 3. Pan-cancer analyses reveal that NCAPD2 overexpression correlates with poor prognosis, immune cell infiltration, and tumor mutational burden across multiple cancer types 4. In pancreatic cancer metastases, NCAPD2 functions as an epigenetic modifier downstream of KLF5, facilitating expression of genes driving migration and epithelial-mesenchymal transition 5. These findings establish NCAPD2 as both a prognostic biomarker and potential therapeutic target.