Monoclonal antibody- clone M7/1 recognizes human endothelial-monocyte-activating polypeptide II (EMAP II). EMAPII is a proinflammatory cytokine and chemoattractant of macrophages and polymorphonuclear lymphocytes. The protein was initially identified as a product of murine methylcholanthrene A-induced fibrosarcoma cells. EMAP II is synthesized as a 34 kDa precursor molecule (proEMAP),- it can run anomalously in SDSpage at 43 kDa, and is enzymatically cleaved to produce a biologically active 22 kDa mature polypeptide. It modulates a range of properties of endothelial cells, monocytes, and neutrophils in vitro, and induces an acute inflammatory reaction and tumor regression in vivo. Later it was found to be anti-angiogenic and capable of induction of apoptosis in proliferation and hypoxic endothelial cells in vitro in tumor vasculature in vivo. EMAP II is released from cells, by a yet unknown mechanism, as pro- and mature EMAP II proteins in response to various forms of cellular stresses, including glucose starvation and hypoxia. Endothelial cells are the main target- for EMAPII and explain the anti-angiogenic property. The anti-tumor effect is expected to a large extent to be mediated through this characteristic. EMAPII is also associated with brain diseases and injury. EMAPII expression is related with leukocytes-infiltrated inflamed tissue and subsequent apoptosis. In solid tumors there is also an immunosuppressive role identified. EMAPII inducing tumor cells induce apoptosis of lymphocytes. EMPAII is considered a marker for microglial cells and macrophages in brain diseases. The distribution of EMAPII and its precursor in biopsies might be applicable as additive diagnostic tool.