They found that neutrophils harvested from myocardium at day 1 following AMI had high expression of pro-inflammatory markers and were polarized by TLR4 activation (termed N1 neutrophils and induced by lipopolysaccharide and interferon-γ), whereas those collected from the heart at days 5–7 post-MI, were anti-inflammatory (termed N2 neutrophils and induced by interleukin-4). This evidence concerns the gene TLR4 and myocardial infarction.