The most important finding in that study was that MCP-1 or shear stress-induced genes like eNOS or Egr-1 are not sufficiently activated to induce collateral artery enlargement in the model of gradual ischemia, since SSF through collaterals is weaker compared to that in an acute ischemia model; additionally eNOS or MCP-1 are less stimulated in gradual or chronic ischemia than in the acute process at the thigh, the place where collateral growth mainly takes place. The gene discussed is EGR1; the disease is ischemia.