Advanced glycation endproducts (AGEs) are primarily known as a complication in diabetic patients through their mediation of the inflammatory response. However, a variety of studies have demonstrated enhanced formation of AGEs in cardiovascular disorders. Despite the large number of AGEs produced during the Maillard reaction, recent focus is on the major non-crosslinking AGE Nepsilon-carboxymethyllysine. Kneyber and colleagues focused on sepsis-induced cardiac dysfunction and investigated whether myocardial inflammation is associated with enhanced cardiac AGE deposition and whether this is further enhanced by mechanical ventilation. They showed that both conditions are associated with enhanced AGE deposition and myocardial inflammation. Therefore, AGEs may participate in the inflammatory response related to cardiac dysfunction in critically ill patients. Moreover, life-saving ventilation stimulates AGE formation in these patients. This interesting study raises the question of whether AGEs in critically ill patients are a driving force of the disease.