In accordance with these studies, a strong acute inflammatory response characterized by neutrophilic influx, increased cytokine secretion (KC, TNF-α, MIP-2, MIP-1α and MCP1), proinflammatory gene expression (KC, MIP-2 and MMP12) and up-regulated GM-CSF production was observed in the mainstream CS model. The gene discussed is CXCL2; the disease is Cowden syndrome 1.