Systemic deletion of SMAD3 does not influence morphology or function under physiological conditions, however, following MI and reperfusion (1 h occlusion, reperfusion for 6 h to 72 h), SMAD3−/− mice demonstrate a short-term (6 h/24 h) reduction of chemokine expression, reduced neutrophil invasion (24 h and 72 h post MI) and reduced fibrotic remodeling of the infarcted heart compared to MI-wildtype mice [107]. The gene discussed is SMAD3; the disease is myocardial infarction.