NMI (N-myc and STAT interactor) is a pleiotropic immune regulator with dual intracellular and extracellular functions. Intracellularly, NMI enhances STAT1 and STAT5-dependent transcription by recruiting CBP/p300 coactivators in response to IL-2 and IFN-γ 1. NMI forms complexes with IFI35 to suppress antiviral responses by promoting IRF7 degradation via TRIM21-mediated ubiquitination 2, while simultaneously inhibiting NF-κB signaling to prevent endothelial dysfunction 3. Extracellularly, macrophage-secreted NMI functions as a damage-associated molecular pattern (DAMP), activating TLR4-NF-κB signaling in adjacent macrophages to promote pro-inflammatory cytokine release during sepsis and tissue injury 4. In cancer biology, NMI acts as a tumor suppressor in lung adenocarcinoma by suppressing PI3K/AKT and COX-2/PGE2 pathways while inhibiting NF-κB acetylation; low NMI expression correlates with poor prognosis 5. NMI also participates in a BRCA1-containing tricomplex that inhibits c-Myc-induced telomerase activation 6. These multifaceted roles position NMI as both a critical immunoregulator and potential therapeutic target for inflammatory and malignant diseases.