The absence or targeting of STAT3 in myeloid cells can enhance CD8+ T cell responses and activate tumor-associated monocytes and DC cells, leading to anti-tumor responses (Herrmann et al., 2010), and inhibiting the pro-angiogenic factors VEGF, bEGF, MMP9, CXCL2 secretion, thereby inhibiting the formation of vascular-like structures (Kujawski et al., 2008). The gene discussed is CXCL2; the disease is neoplasm.