IRF2 is a member of the IRF family of transcription factors, mainly functioning as a transcriptional repressor. It binds to the interferon-sensitive response elements (ISREs) and competes for binding sites with the other IRF transcription factors, such as IRF1 and IRF9. Mice deficient in IRF2 spontaneously develop skin inflammation due to excessive activation of CD8+ T lymphocytes. Further, the severely reduced number of mature NK cells in IRF2-deficient mice suggests that IRF2 is required for normal NK cell development. IRF2 contains a latent activation domain that can act as a transcriptional activator and has been revealed to positively regulate Histone H4 and VCAM-1 gene expression.