IRF8 and neoplasm: For instance, the binding sites of PU.1, CCAAT-enhancer-binding protein (CEBP), and interferon regulatory factor (IRF)-8 of Ly6Chi monocytes were less accessible after MI, which impaired myeloid cell differentiation and transcriptionally inhibited numerous genes regulated by PU.1, CEBP and IRF-8 such as CD40 and CD86 genes involved in T cell activation, resulting in an immunosuppressive phenotype that persists in tumor monocytic myeloid-derived suppressor cells (mMDSCs) [26].