Mice with specific deletion of Tgfbr1 or Tgfbr2 in cardiomyocytes (αMHC-MerCreMer; Tgfbr1flox/flox or αMHC-MerCreMer; Tgfbr2flox/flox mice, tamoxifen treatment: 2-4 weeks before MI) are protected against MI-dependent, early onset mortality due to wall rupture and show a marked decrease in neutrophil recruitment and accompanying metalloproteinase-9 activation after MI (non-reperfused) [92]. This evidence concerns the gene TGFBR2 and myocardial infarction.