In a model of acute myocardial infarction, IL-10 administration significantly suppressed proinflammatory cytokine production, MMP-9 activity, and inflammatory cell infiltration of the myocardium, with a resultant decrease in cardiac fibrosis.7 This resulted in improved left ventricular function and diminished pathological remodeling, including smaller infarct size and less wall thinning. The gene discussed is IL10; the disease is myocardial infarction.