ZNF24 is a zinc finger transcription factor required for oligodendrocyte myelination and CNS development. During differentiation, it promotes the transition of oligodendrocytes from premyelinating to myelinating states and maintains progenitor cell populations by regulating the cell cycle. ZNF24 binds the DNA sequence 5'-TCAT-3' and functions as a transcriptional repressor in vitro, though it also exhibits activating functions in specific contexts. Across multiple cancer types, ZNF24 acts as a tumor suppressor. It represses vascular endothelial growth factor (VEGF) transcription by directly binding an 11-bp promoter fragment, thereby inhibiting tumor angiogenesis 1. In bladder cancer, higher ZNF24 expression predicts better prognosis; reduced expression correlates with poor outcomes in ovarian serous carcinoma and clear cell renal carcinoma 2, 3, 4. In lung adenocarcinoma, loss of ZNF24 expression permits KRAS mutation-driven immune escape through increased PD-L1 expression 5. ZNF24 protein stability is regulated by crosstalk between SUMOylation and ubiquitination; SUMOylation at lysine-27 protects against proteasomal degradation by CUL3 2. Clinically, ZNF24 inhibition represents an emerging therapeutic strategy. A 2025 study identifies daptomycin as the first reported inhibitor of ZNF24, with potential to enhance CD8+ T cell immunity when combined with anti-PD-L1 antibodies in KRAS-mutated lung adenocarcinoma 5. Bevacizumab combined with BMI1 inhibitors may also benefit NSCLC by restoring ZNF24-mediated VEGF suppression 6.