IRF2 (interferon regulatory factor 2) is a transcription factor that plays complex dual roles in immune regulation and disease pathogenesis. As a member of the IRF family, IRF2 functions as both a transcriptional activator and repressor with sequence-specific DNA-binding activity 1. In cancer contexts, IRF2 exhibits tumor suppressor properties, as demonstrated in colorectal cancer where KRAS-mediated repression of IRF2 leads to immune suppression through the CXCL3-CXCR2 axis, and higher IRF2 expression correlates with improved anti-PD-1 therapy responsiveness 2. However, IRF2 also promotes immune exhaustion by driving interferon-mediated CD8+ T cell dysfunction, with IRF2 deletion enabling sustained T cell effector functions and enhanced tumor control 3. IRF2 is essential for normal immune cell development, particularly NK cell differentiation and functional maturation, where knockdown severely impairs cell proliferation and cytotoxic capacity 4. In hepatocellular carcinoma, IRF2 activation occurs upon β-catenin suppression, contributing to immune regulatory responses 5. Additionally, IRF2 can function as an oncogene in certain contexts, directly promoting expression of proteins like CENP-N in nasopharyngeal carcinoma 6 and POSTN in intervertebral disc degeneration 7. The balance between IRF2's tumor suppressor and oncogenic functions appears context-dependent and represents a potential therapeutic target.