It has recently been shown that inhibition of TLR2 decreased angiotensin II-induced cardiac fibrosis through a potent reduction in the tissue infiltration by inflammatory cells, particularly macrophages [264], and another study found that MMP28 regulated the fibrotic response to myocardial infarction in mice, with MMP28 deletion exacerbating cardiac fibrosis, an effect mediated by inhibition of M2 macrophage activation [265]. The gene discussed is MMP28; the disease is myocardial infarction.