The miR‐29 family members are potent inhibitors of cardiac fibrosis and play a key role in cardiac remodeling following cardiomyocyte injury.31 Plasma miR‐29a upregulation has been reported following myocardial injury, where the degree of mR‐29a upregulation was associated with the extent of late remodeling post‐acute myocardial infarction.24 miR‐29b, reported herein, targets many genes involved in the extracellular matrix (ECM), such as fibronectin, collagen, and matrix metalloproteinases. The gene discussed is FN1; the disease is myocardial infarction.