Application of TIMP2 leads to enhanced synaptic plasticity and improved cognitive function in mice;  TIMP2 deficiency inhibits cardiac remodeling processes after myocardial infarction in mice via inhibition of membrane type 1 matrix metalloproteinase;  involved in homing mechanisms of human mesenchymal stem cells;  elevated plasma levels of TIMP1, TIMP2 and TIMP4 have been associated with higher risk for major adverse cardiac events after acute myocardial injury in humans. The gene discussed is TIMP4; the disease is myocardial infarction.