LCOR (ligand dependent nuclear receptor corepressor) functions as a transcriptional regulator with dual corepressor and coactivator activities depending on cellular context. As a corepressor, LCOR inhibits ligand-dependent transcription activation by nuclear receptors including estrogen, progesterone, glucocorticoid, retinoic acid, and vitamin D receptors 1. However, LCOR also demonstrates unexpected transcriptional activator functions, particularly as a master regulator of antigen processing/presentation machinery (APM) genes through binding to IFN-stimulated response elements independently of IFN signaling 2. LCOR interacts with other transcriptional regulators like RUNX1 and forms complexes with corepressors such as HDAC3 to modulate gene expression 34. In cancer contexts, LCOR shows tissue-specific roles: it enhances tumor immunogenicity and immune checkpoint blockade responsiveness in triple-negative breast cancer 2, while high cytoplasmic LCOR expression correlates with longer survival in endometrial cancer 1. LCOR also regulates lipid metabolism in clear cell renal cell carcinoma by relieving RUNX1-mediated repression of PLCL1 3. Additionally, LCOR contributes to hematopoietic stem cell specification, being one of seven transcription factors sufficient to convert hemogenic endothelium into functional hematopoietic stem cells 5.