ANP32E is a histone chaperone that mediates genome-wide removal of histone H2A.Z from nucleosomes, particularly at enhancer and insulator regions, and inhibits protein phosphatase 2A activity. The protein is expressed widely across human tissues including peripheral blood leukocytes, colon, small intestine, prostate, thymus, spleen, skeletal muscle, liver, and kidney. At the molecular level, ANP32E functions through its N-terminal leucine-rich repeat domain and C-terminal low-complexity acidic region to regulate chr1 structure and transcription. Recent evidence suggests ANP32E can be exploited by influenza A viruses as a host factor when polymerase dimerization is altered by specific mutations, enabling viral adaptation 1. Additionally, ANP32E serves as a cofactor for influenza polymerase assembly in mammalian cells 2. Clinically, ANP32E overexpression associates with poor prognosis across multiple cancer types. In triple-negative breast cancer, high ANP32E expression correlates with worse overall survival and increased disease recurrence, with ANP32E promoting G1/S transition through E2F1 induction 3. In pancreatic ductal adenocarcinoma, ANP32E expression predicts poor gemcitabine efficacy and worse outcomes, with knockdown sensitizing tumor cells to chemotherapy 4. In esophageal cancer, ANP32E promotes progression and paclitaxel resistance via p53/SLC7A11-regulated ferroptosis 5. In breast cancer, ANP32E-driven H2A.Z turnover increases transcription-replication conflicts and R-loop accumulation, creating vulnerability to ATR inhibitors 6.