For example, pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) have been shown to upregulate uPAR, as well as uPA secretion, in various cell types such as monocytes, endothelial cells, and tumor cells [80], which in turn can facilitate JAK1/2 activation and STAT3 phosphorylation, thereby amplifying inflammatory signaling cascades. The gene discussed is STAT3; the disease is neoplasm.