ZNF366 is a zinc finger transcription factor that functions as a potent corepressor of estrogen receptor-alpha (ERα) signaling 1. The protein mediates transcriptional repression through interactions with multiple corepressor complexes, including CtBP and histone deacetylases, which facilitate chr5 remodeling and histone modification to inhibit estrogen-responsive gene expression 1. Beyond estrogen signaling, ZNF366 regulates dendritic cell development, with evidence suggesting it functions as a transcription factor controlling mo-DC (monocyte-derived dendritic cell) differentiation during inflammation 2. Additionally, ZNF366 acts as a negative regulator of glucocorticoid receptor function 3. ZNF366 has emerging disease relevance across multiple conditions. Genome-wide association studies identified ZNF366 as a stress-sensitivity locus associated with major depressive disorder susceptibility 3. The gene was also implicated as a candidate asthma locus in African-ancestry populations, with genetically regulated expression in nasal epithelium and CD4+ T cells affecting asthma risk through inflammatory mechanisms 4. Furthermore, ZNF366 variants show association with hemostatic factor regulation and hemorrhagic transformation risk after stroke thrombolytic treatment 5. These findings suggest ZNF366 participates in coordinating stress responses, immune regulation, and hemostatic balance across multiple physiological systems.