ZNF687 is a zinc finger transcription factor with diverse roles in bone development, hematopoiesis, and cancer biology. In bone biology, ZNF687 mutations are associated with Paget disease of bone (PDB), a disorder characterized by increased bone resorption and excessive bone formation 1. ZNF687 is regulated by bone-associated transcription factors including DLX5, NFκB, PU.1, and SOX9, with DNA methylation modulating their activity on ZNF687 promoters 2. Notably, disease-causing variants cluster within ZNF687's nuclear localization signal, suggesting this domain is functionally critical 3. In hematopoiesis, ZNF687 functions as a lineage-preferential transcription factor regulating neutrophil development by recruiting the BRD4-SMRT corepressor complex to negatively regulate gfi1aa 4. Beyond bone, ZNF687 acts as an oncogene in multiple cancers. In hepatocellular carcinoma, elevated ZNF687 confers tyrosine kinase inhibitor resistance and poor prognosis 5. In lung adenocarcinoma, ZNF687 overexpression promotes proliferation and epithelial-mesenchymal transition via PI3K/AKT pathway activation 6. In colorectal cancer, FTO-mediated ZNF687 drives tumor progression through the Wnt/β-catenin pathway 7. ZNF687 dysregulation represents a therapeutic target across multiple disease contexts.