This is also reflected in the observation that overexpression of RAGE and reduced sRAGE correlates with chronic inflammation in inflammatory diseases such as atherosclerosis and diabetes.22 Our preliminary observation of alterations in sRAGE expression in mouse and human disease suggests there may be merit in looking at both calprotectin and sRAGE to better predict whether calprotectin and other RAGE ligands are indeed able to drive pro-inflammatory signals. The gene discussed is AGER; the disease is atherosclerosis.